Esophageal varices

Esophageal varices

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Varicose veins are dilated blood vessels usually esophagus or stomach. Only if they break and cause symptoms singereaza. One of the notable consequences of portal hypertension is the formation of collateral circulation deep, expressed clinically by the occurrence of esophageal and gastric varices, which shows a high risk of bleeding.
Over 50% of those diagnosed with cirrhosis develop esophageal varices In a year and 90% in 10 years, and 30-50% of them will bleed at some point with a risk of recurrent singerarii 70%. Burglary of upper digestive bleeding esophageal varices is a complication with poor prognosis, 30-50% died in the first hemorrhage and 70% in the second.
Esophageal varices are usually asymptomatic, but may have only one symptom of great importance, because it puts the patient's life in danger: upper gastrointestinal bleeding, usually manifested by massive haematemesis with or without melena.
Endoscopy is the ideal method for early assessment of varicose veins and their classification in risk groups, and in case of endoscopic treatment of bleeding immediately. The risk of bleeding depends primarily on the size of varices and Child class which is placed in the patient. During endoscopy should specify singerarii undoubtedly singerarii source and presence of other potential bleeding lesions. The moment when endoscopy should be performed in case of bleeding: when the patient is stable hemodynamically and gastric contents is discharged, under conditions of monitoring and pulse oximetry.
Treatment consists of hospitalization in intensive care, hemodynamics and electrolyte rebalancing, and hemostasis. Haemostasis may be drug, vasoactive drugs and / or endoscopic: sclerosis of bleeding vessels, embolization with various agents, inert, electrocoagulation, photocoagulation, clipped, metallic.
Pathogenesis
Portal flow obstruction at any level leads to increased portal pressure. Normal pressure in the portal vein is 5-10 mmHg because vascular resistance in liver sinusoids is small. A high pressure> 10 mmHg relaxes veins proximal capillary blockage and increase the pressure in the veins draining obstructed organs: esophagus and stomach.
Because the portal vein valves do not show resistance to any level between the heart and vessels splanhice result intro right retrograde flow of blood and increased pressure transmission. Anastomoses connecting the portal and systemic circulation to expand to allow blood to bypass obstruction in the systemic circulation.
Studies have demonstrated the role of endothelin-1 and nitric oxide in the pathogenesis of hypertension and esophageal varices. Endothelin-1 is a potent vasoconstrictor synthesized by sinusoidal endothelial cells involved in the increase of portal pressure and liver fibrosis development. NO is a vasodilator also synthesized by sinusoidal endothelial cells. In cirrhotic liver production of NO and NO synthase activity is low.
Obstruction and resistance can occur at three levels in relation to hepatic sinusoids: Presinusoidale-blocking veins (portal vein thrombosis, schistosomiaza, primary biliary cirrhosis) Postsinusoidale-blocking veins (Budd-Chiari syndrome, veno-occlusive disease) Sine-blocking (cirrhosis), characterized by increased venous gardient-loaded.
Varicose gastroesofageale have two sources of blood, one is left gastric vein. The second is the hilum splenic, short gastric veins.
Hepatic microcirculation research studies have identified several mechanisms that explain the increased intrahepatic vascular resistance: Sinus-size reduction by hepatomegaly -Impaired elastic properties of the walls by the deposition of collagen in the sinusoidal space DISS Regenererea-compression nodular hepatic venules -Central venous lesions by perivenous fibrosis -Veno-occlusive changes Perisinusoidal by blocking inflammation-portal, portal fibrosis and necrosis.
The following factors increase the risk of bleeding varices: -Size veins Endoscopic this red-wall signs Child-classification, especially this increases the risk of bleeding ascites Active consumption of alcohol, chronic liver disease Local-pathological changes of the esophagus: gastro-esophageal reflux. There is an association between esophageal bleeding and bacterial infections.