Bülent Ünal, Koray Kultutürk, Turgut Pişkin, Emrah Otan, Cemalettin Aydın, Sezai Yılmaz

Özofagus Varis Kanamalarına Güncel Yaklaşımlar

Özofagus varisleri portal kan basıncının artmasına bağlı, özofagusun distalinde gastrik venler ile azigos ven arasında geşilen kolaterallerdir. Portal ven basıncının 10 mm Hg’nin üzerinde olmasına portal hipertansiyon denilir. Portal hipertansiyonda portal ven – hepatik ven basınç gradiyenti artmıştır. Bu durum “klinik olarak önem arz eden portal hipertansiyon” olarak adlandırılmaktadır ve en sık karaciğer sirozunda karşılaşılır. Karaciğer sirozu olan hastalarda asit oluşumu ve özofagus varis kanamalarının olması ilerlemiş hastalık belirtileridir ve bu hastaların beklenen yaşama süresi oldukça kısalmıştır. Kompanze sirozlu hastaların %30’unda dekompanze sirozlu hastaların %60-70’inde özofagus varisi gelişmektedir. Varisi olmayan sirotik hastalarda yıllık varis oluşum hızı %4-12 dolayındadır. Özofagus varis kanaması yüksek rekürrens, mortalite ve morbidite oranına sahip acil medikal tedavi gerektiren hastalıklardan biridir. Özofagus varis kanamaları üst gastrointestinal sistem kanamalarının yaklaşık %10’unu oluştururlar ve sirozlu hastalarda başlıca mortalite nedenlerindendir. Özofagus varis kanaması, endoskopik olarak özofagus varisi saptanan sirotik hastaların %30'unda gelişmektedir. İlk kanama epizodunun mortalitesi % 25-70 arasında değişmektedir ve ilk kanama sonrası varislerin % 75-80’inde altı ay ya da bir yıl içinde yeniden kanama meydana gelir. Varis çapı, grade, kırmızı noktalanmalar ve siroz derecesi varis kanaması riskini arttıran faktörlerdir. Grade 1 varislerde kanama riski %8 iken grade arttıkça kanama riski 4-5 kat artmaktadır. Özofagus varis kanamalarında tedavinin temelini farmakolojik, endoskopik ve antibiyotik tedavisi oluşturur. Bu çalışmada özofagus varis kanamalarına güncel yaklaşımlar ele alınmıştır.

Anahtar Kelimeler:

Özofagus Varis Kanaması, Portal Hipertansiyon, Siroz

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Esophageal varices are collateral veins at the distal esophagus between gastric and azygos veins arising following increased portal pressure. Vein pressure above 10 mmHg is regarded as portal hypertension, in which portal vein-hepatic vein pressure gradient is increased. This status is seen as "clinically important portal hypertension" and it is most common in liver cirrhosis. Acid and esophageal variceal bleeding is the result of portal hypertension, which are the signs of advanced disease with poorer survival rates. Esophageal varices develop in 30% of the patients with compensated cirrhosis and 60-70% of the patients with decompensated cirrhosis. Varice development incidence is around 4-12% in cirrhotic patients without varices. Esophageal variceal hemorrhage has high recurrence, mortality, and morbidity rates requiring immediate medical treatment and these constitute approximately 10% of upper gastrointestinal bleeding, which is one of the major causes of mortality in patients with cirrhosis. Bleeding develops in 30% of the cirrhotic patients with esophageal varices diagnosed during endoscopy. The mortality of the first bleeding episode ranges from 25 to 70% and after the first bleeding episode rebleeding occurs at a rate of 75-80% in six to twelve months. Variceal diameter, grade, degree of red dots, and cirrhosis are among the factors that increase the risk of variceal bleeding. The risk of bleeding in Grade 1 varices is 8% and a higher grade increases the risk of bleeding four to five folds. Pharmacological endoscopic and antibiotic treatment constitutes the basis for esophageal variceal bleeding treatment. In this study, we aimed to evaluate the current approaches to esophageal variceal bleeding

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