Varices

Varices

Hepatic portal vein Illustration (Anatomy recall)

Esophageal Varices

Background The portal vein carries approximately 1500 mL /min of blood from the: small and large bowel the spleen and the stomach to the liver

Esophageal Varices Background Obstruction of portal venous flow, whatever the etiology, results in a rise in portal venous pressure

The response to increased venous pressure is the development ► of a collateral circulation diverting the obstructed blood flow to ► the systemic veins

Esophageal Varices Background These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting : 1) the portal venous system and 2) the superior and inferior vena cava

Esophageal Varices Background High portal pressure is the main cause of the development of portosystemic collaterals However, other factors such as active angiogenesis also may be involved

Esophageal Varices Background The most important portosystemic anastomoses are the gastroesophageal collaterals Draining into the azygos vein, these collaterals include esophageal varices which are responsible for the main complication of portal hypertension ► massive upper GI hemorrhage

Esophageal Varices Background The most common causes of upper GI bleeding are: duodenal and gastric ulcers responsible for 35% and 20% of cases, respectively

Bleeding from esophageal varices is responsible for only 5-11% upper GI bleeding (incidence varies depending on geographic location)

Esophageal Varices Background Other causes for upper GI bleeding are: 1) acute gastric erosions/hemorrhagic gastritis (18%) 2) Mallory-Weiss tears (10%) 3) gastric carcinoma (6%) and 4) other causes (6%)

Pathophysiology Obstruction of the portal venous system at any level leads to increased portal pressure Normal pressure in the portal vein is 5-10 mm Hg Because the vascular resistance in the hepatic sinusoids is low An elevated portal venous pressure (>10 mm Hg) * distends the veins proximal to the site of the block and * increases capillary pressure in organs drained by the obstructed veins

Esophageal Varices Pathophysiology Because the portal venous system lacks valves, resistance at any level between the right side of the heart and the splanchnic vessels results in: * retrograde flow of blood and * transmission of elevated pressure

Esophageal Varices Pathophysiology The anastomoses connecting the: * portal and * systemic circulation may enlarge to allow blood to: * bypass the obstruction and * pass directly into the systemic circulation

Esophageal Varices Pathophysiology Obstruction and increased resistance can occur at 3 levels in relation to hepatic sinusoids, as follows: 1) Presinusoidal venous block: e.g.: portal vein thrombosis schistosomiasis primary biliary cirrhosis These lesions are characterized by: * elevated portal venous pressure * but a normal wedged hepatic venous pressure (WHVP)

Esophageal Varices Pathophysiology 2) Postsinusoidal obstruction e.g.: Budd-Chiari syndrome venoocclusive disease * in which the central hepatic venules are the primary site of injury * WHVP characteristically is elevated

Esophageal Varices Pathophysiology 3) Sinusoidal obstruction e.g.: cirrhosis * is characterized by increased hepatic venous pressure gradient (HVPG) * with WHVP being equal to portal venous pressure

Esophageal Varices Pathophysiology Gastroesophageal varices have 2 main inflows: the first is the: 1) * left gastric (or coronary vein) The other major route of inflow is the: 2) * splenic hilus, through the short gastric veins The gastroesophageal varices are important because of their propensity to bleed

Esophageal Varices Pathophysiology The following are risk factors for variceal hemorrhage: ► Variceal size: The larger the varix, the higher the risk of: rupture and bleeding Remember: However, patients may bleed from small varices too

Esophageal Varices Pathophysiology The following are risk factors for variceal hemorrhage: ► The presence of endoscopic red color signs e.g.: (A) red whale markings; (B) cherry red spots

►The presence of ascites, increases the risk of hemorrhage

Esophageal Varices Pathophysiology The following are risk factors for variceal hemorrhage: A well-documented association exists between: variceal hemorrhage and bacterial infections and this may represent a causal relationship

Esophageal Varices Infection could trigger variceal bleeding by a

number of mechanisms, including the following:

► Active alcohol intake in patients with chronic alcoholrelated liver diseases ► Local changes in the distal esophagus e.g.: gastroesophageal reflux have been postulated to increase the risk of variceal hemorrhage

Esophageal Varices Pathophysiology The release of endotoxin into the systemic circulation ►

► Worsening of hemostasis

Frequency In Western countries alcoholic and viral cirrhosis are the leading causes of: portal hypertension and esophageal varices Hepatitis B is endemic in the * East and Southeast Asia * Africa and * other countries in the Middle East

Esophageal Varices Frequency Schistosomiasis is an important cause of portal hypertension * African and * Asian countries Hepatitis C is becoming a major cause of liver cirrhosis worldwide

Esophageal Varices Frequency 30% of patients with compensated cirrhosis and 60-70% of patients with decompensated cirrhosis have gastroesophageal varices at presentation

Remember The risk of bleeding from esophageal varices is 30% in the first year after identification

Esophageal Varices Mortality/Morbidity Patients who have bled once from esophageal varices have a 70% chance of rebleeding Approximately one third of further bleeding episodes are fatal

Esophageal Varices Sex In females alcoholic liver disease viral hepatitis venoocclusive disease and primary biliary cirrhosis usually are responsible In males alcoholic liver disease and viral hepatitis usually are responsible

Esophageal Varices Age Portal vein thrombosis and Secondary biliary cirrhosis are the most common causes of varices in children Cirrhosis is the most common cause of esophageal varices in adults

Esophageal Varices Clinical Presentation History 1) Symptoms of liver disease Weakness Tiredness Malaise Anorexia

Esophageal Varices Clinical Presentation History 2) Symptoms of liver disease Sudden and massive bleeding with ►►shock on presentation ► Nausea and vomiting

Esophageal Varices Clinical Presentation History 3) Symptoms of liver disease Weight loss Abdominal discomfort and Pain - Usually felt in the right hypochondrium

Esophageal Varices Clinical Presentation History 4) Symptoms of liver disease * Jaundice or dark urine * Edema and abdominal swelling * Pruritus * Spontaneous bleeding

Esophageal Varices Clinical Presentation History Encephalopathy symptoms: * Disturbance of the sleep-wake cycle * Deterioration in intellectual function * Memory loss * Impotence and sexual dysfunction * Muscle cramps - Common in patients with cirrhosis

Esophageal Varices Past medical history

►Previous jaundice suggests the possibility of: a previous acute hepatitis hepatobiliary disorder or drug-induced liver disease ► Recurrence of jaundice suggests the possibility of: reactivation infection with another virus or the onset of hepatic decompensation

Esophageal Varices Past medical history ► blood transfusion ► schistosomiasis

Family history of hereditary liver disease such as ► Wilson disease