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The liver is a unique organ in that it has a dual blood supply: portal venous and hepatic arterial. 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. The left gastric, or coronary, vein drains the distal esophagus and lesser curvature of the stomach, generally entering the portal vein near its origin.

Hepatic blood flow averages 1500 mL/minute, which represents about 25% of the cardiac output. The portal vein contributes two thirds of the total hepatic blood flow, whereas hepatic arterial perfusion accounts for more than half of the liver's oxygen supply.

I. Increased resistance to flow
A. Prehepatic (portal vein obstruction) 1. Congenital atresia or stenosis 2. Thrombosis of portal vein 3. Thrombosis of splenic vein 4. Extrinsic compression (eg, tumors)

B. Hepatic 1. Cirrhosis a. Portal cirrhosis (nutritional, alcoholic, Lannec) b. Postnecrotic cirrhosis c. Biliary cirrhosis d. Others (Wilson disease, hemochromatosis) 2. Acute alcoholic liver disease 3. Chronic active hepatitis 4. Congenital hepatic fibrosis 5. Idiopathic portal hypertension (hepatoportal sclerosis) 6. Schistosomiasis 7. Sarcoidosis

C. Posthepatic 1. Budd-Chiari syndrome (hepatic vein thrombosis) 2. Veno-occlusive disease 3. Cardiac disease a. Constrictive pericarditis b. Valvular heart disease c. Right heart failure II. Increased portal blood flow A. Arterial-portal venous fistula B. Increased splenic flow 1. Banti syndrome 2. Splenomegaly (eg, tropical splenomegaly, myeloid metaplasia)

Pathophysiology Portal venous pressure normally ranges from 7 to 10 mm Hg. In portal hypertension, portal pressure exceeds 10 mm Hg, averaging around 20 mm Hg and occasionally rising as high as 5060 mm Hg. Since pressure in the portal venous system is determined by the relationship Pressure = Flow x Resistance, portal hypertension could result either from increased volume of portal blood flow or increased resistance to flow. Nearly all clinically relevant cases result from increased resistance, although the site of the resistance varies in different diseases. In alcoholic liver disease, the abnormal resistance is predominantly postsinusoidal, as indicated by the results of wedged hepatic vein pressure studies. The causes of increased resistance in this disease are thought to be (1) distortion of the hepatic veins by regenerative nodules and (2) fibrosis of perivascular tissue around the hepatic veins and the sinusoids.

Portal hypertension is defined by a portal pressure above 5 mm Hg. Somewhat higher pressures (8-10 mm Hg) are required to stimulate portosystemic collateralization. Collateral vessels usually develop where the portal and systemic venous circulations are in close proximity. The collateral network through the coronary and short gastric veins to the azygos vein is the most important one clinically because it results in formation of esophagogastric varices; however, other sites include a recanalized umbilical vein from the left portal vein to the epigastric venous system (caput medusae), retroperitoneal collateral vessels, and the hemorrhoidal venous plexus.

Alcohol induces a specific cytochrome P450 in the liver (ie, P450 2E1) that participates in its metabolism to acetaldehyde, which has a number of deleterious effects, including antibody formation, decreased DNA repair, enzyme inactivation, and alterations in microtubules, mitochondria, and plasma membranes. Acetaldehyde also promotes glutathione depletion, free radical mediated toxicity, lipid peroxidation, and hepatic collagen synthesis. Hepatic steatosis and alcoholic hepatitis are stages of alcoholic liver injury that may precede cirrhosis. Alcoholic hyalin, a glycoprotein, accumulates in centrilobular hepatocytes of patients with alcoholic hepatitis. There is some evidence that immunologic responses to alcoholic hyalin may be important in the pathogenesis of cirrhosis.

Collagen deposition in cirrhosis results from increased fibroblastic activity as well as from repair following hepatocellular injury and necrosis. The ultimate result is a liver containing regenerative nodules and connective tissue septa linking portal fields with central canals


Haematemesis Ascites Hemorrhoids Weakness Signs of liver failurejaundice, capute medusae, spider angiomata, fetor hepaticus, asterixis, ascites, hemorrhoids, palmar erythema, temporal wasting, duputrens contracture, gynaecomastia, testicular atrophy, splenomegaly

Variceal bleeding Ascites Encephalopathy Hepatorenal syndrome End-stage liver disease


History and Physical Examination ->constitutional complaints such as weight loss, malaise, and weakness ->past history of chronic alcoholism, hepatitis, complicated biliary disease, or exposure to hepatotoxins leads one to include cirrhosis in the differential diagnosis. ->physical examination - spider angiomas, palmar erythema, testicular atrophy, gynecomastia, spleenomegaly ->signs of hepatic functional decompensation or advanced portal hypertension, such as jaundice, ascites, palpation of a firm irregular liver edge, dilated abdominal wall veins, and impairment of mental status or the presence of asterixis (liver flap)

Laboratory Tests
Blood group Hb% TLc-DLc-degree of thrombocytopenia has been found to be a quite accurate predictor of the presence of esophageal varices Liver function tests, Alkaline po4 Serum electrolytes-hyponatremia, hypokalemia, and metabolic alkalosis. Albumin- hypoalbunemia Platelet count <50000 International Normalized Ratio - increases Serologies for viral hepatitis Iron indices Antinuclear antibody Antimitochondrial antibody, antismooth muscle antibody Alpha1-antitrypsin deficiency Ceruloplasmin

Liver Biopsy Percutaneous liver biopsy is a useful technique for establishing the cause of cirrhosis and for assessing activity of the liver disease. Percutaneous liver biopsy is not done when either coagulopathy or moderate ascites is present Laparoscopic biopsy reduces the false-negative rate for diagnosing cirrhosis as compared with the blind biopsy techniques.

Measurement of Hepatic Functional Reserve

The single most life-threatening complication of portal hypertension, responsible for about one third of all deaths in patients with cirrhosis. About one half of the deaths are due to uncontrolled bleeding. The risk for death from bleeding is mainly related to the underlying hepatic functional reserve. Patients with extrahepatic portal venous obstruction and normal hepatic function rarely die from bleeding varices, whereas those with decompensated cirrhosis (Child-Pugh class C) may face a mortality rate in excess of 50%.

Varices in the distal esophagus and proximal stomach are a component of the collateral network that diverts high-pressure portal venous flow through the left and right gastric veins and the short gastric veins to the azygous system. Esophagogastric varices do not bleed until portal pressure exceeds 12 mm Hg, and then they bleed in only one third to one half of patients. The pathophysiology of variceal rupture is based on Laplace's law. Laplace's law states that variceal wall tension is directly related to transmural pressure and varix radius and inversely related to variceal wall thickness, thus combining all three of these variables.

The three key variables that are predictive of variceal bleeding are Child-Pugh class, variceal size, and the presence and severity of red wale markings (indicative of epithelial thickness). especially important when considering prophylactic therapy (treatment of varices that have not previously bleed)

Treatment of the Acute Bleeding Episode

Resuscitation and Diagnosis restoration of circulating blood Volume status is assessed by central venous pressure measurements, urinary output. replacement of clotting factors (with fresh frozen plasma, vitamin K, and platelets) must be employed aggressively. Endoscopy to determine the cause of bleeding is performed as soon as the patient is stabilized. prophylactic antibiotics are initiated. They have been shown to decrease the infection rate by more than 50%, decrease rebleeding, and improve survival.

Octreotide is given as an IV bolus of 50 mg followed by an infusion of 25 to 50 mg/hour for 2 to 3 days If vasopressin is used, it needs to be given as an initial bolus of 20 units over 20 minutes followed by an infusion of 0.2 to 0.4 units/minute. Because of the adverse systemic effects of vasopressin, nitroglycerine is simultaneously infused at an initial rate of 40 mg/minute and then titrated to achieve blood pressure control.
Sengstaken-Blakemore tube oral or nasogastric lactulose

Endoscopic Treatment
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. In the acute setting, sclerotherapy and band ligation have been shown to be equally efficacious. Ligation is associated with fewer complications, but it is more difficult to do in the acutely bleeding patient. Both techniques require a skilled endoscopist and stop the bleeding in 80% to 90% of patients.

->Minor complications of sclerotherapyretrosternal chest pain, esophageal ulceration, and fever. ->More serious complications, which account for the 1% to 3% mortality rate of this procedureesophageal perforation, worsening of variceal hemorrhage, and aspiration pneumonitis. (Failure of endoscopic treatment is declared when two sessions fail to control hemorrhage.)

Transjugular Intrahepatic Portosystemic Shunt

->Minimally invasive procedure ->TIPS is a technique that accomplishes portal decompression without an operation. ->Because of the complexity of the procedure, an experienced interventional radiologist is required. ->Access is gained to a major intrahepatic portal venous branch by puncture through a hepatic vein. A parenchymal tract between hepatic and portal veins is then created with a balloon catheter, and a 10-mm expandable metal stent is inserted, thereby creating the shunt. Which is expandable to diameter that reduces portosystemic gradient <12 mm Hg.

1. bleeding refractory to medical and endoscopic management 2. as a short-term bridge to liver transplantation for patients in whom endoscopic treatment has failed 3. refractory ascites 4. budd chiary syndrome 5. hepatorenal syndrome
Disadvantages1. Post procedure encephalopathy(25%) 2. Stenosis (2/3rd)

Contra indications Absolute contraindications right-sided heart failure polycystic liver disease. Relative contraindications portal vein thrombosis, hypervascular liver tumors,, encephalopathy which can be worsened by diversion of portal flow

Portosystemic Shunts
the most effective means of preventing recurrent hemorrhage in patients with portal hypertension. These procedures are effective because they all, to some degree, decompress the portal venous system by shunting portal flow into the low-pressure systemic venous system.

A) Nonselective shunts

completely divert portal flow The end-to-side portacaval shunt (Eck fistula), The side-to-side portacaval shunt, large-diameter interposition shunts, the conventional splenorenal shunt

the portal and systemic venous systems in a side-to-side fashion. Therefore, these procedures decompress both the splanchnic venous circulation and the intrahepatic sinusoidal network. Because the liver and intestines are both important contributors to ascites formation, side-to-side portosystemic shunts are the most effective shunt procedures for relieving ascites as well as preventing recurrent variceal bleeding. Because they completely divert portal flow like the end-to-side portacaval shunt, however, side-to-side shunts also accelerate hepatic failure and lead to frequent postshunt encephalopathy

-Synthetic grafts or autogenous vein (internal jugular

vein) -The conventional splenorenal shunt consists of

anastomosis of the proximal splenic vein to the renal vein. Splenectomy is also done.

B) Selective Shunts Selective shunts lower pressure in the gastroesophageal venous plexus while preserving blood flow through the liver via the portal vein. The distal splenorenal (Warren) shunt involves anastomosing the distal (splenic) end of the transected splenic vein to the side of the left renal vein, plus ligation of the major collaterals between the remaining portal and isolated gastrosplenic venous system. The latter step involves division of the gastric vein, the right gastroepiploic vein, and the vessels in the splenocolic ligament shunt does not improve ascites selective shunt (Inokuchi shunt) consists of joining the left gastric vein to the inferior vena cava by a short segment of autogenous saphenous vein.

Devascularization Operations The objective of devascularization is to destroy the venous collaterals that transport blood from the high-pressure portal system into the veins in the submucosa of the esophagus the upper two thirds of the stomach is devascularized, and selective vagotomy, pyloroplasty, and splenectomy are performed