İskemik Hepatit
Özet
İskemik hepatit (şok karaciğeri), kalp, dolaşım veya solunum yetmezliği sonucu gelişen, sentrilobüler karaciğer hücre nekrozu ve serum aminotransferazlarında (AST, ALT) ani artışla karakterize, akut karaciğer hasarının en yaygın nedenidir. Karaciğerin portal ven ve hepatik arterden çift kan alması ile yüksek geçirgenlikli sinüzoidal yapısı organı hipoksiye karşı korusa da kalp yetmezliği (%39-70), sepsis (%15-30) ve solunum yetmezliği (%15) vakaların %90’ından fazlasının altta yatan nedenidir. Genellikle subklinik seyreden bu tabloda klinik bulgular nadirdir; hastaların çoğunda şok hali ve altta yatan kalp yetmezliği semptomları (sağ üst kadran ağrısı, hepatomegali) görülür. Laboratuvarda aminotransferazlar ve LDH hızla yükselip ilk 3 günde %50'den fazla düşerken, ALT/LDH oranının 1.5'in altında olması ve INR'nin 2'den büyük olmasının kötü prognoza işaret etmesi tipiktir. Tanı için biyopsi nadiren gerekir, tanı kriterleri akut yetmezlik kliniği ve aminotransferazların 20 katından fazla artmasıdır. Spesifik bir tedavisi olmayan ve yönetimi altta yatan hastalığın düzeltilmesine dayanan iskemik hepatitte mortalite oranı %56 gibi yüksek bir düzeydedir.
Ischemic hepatitis (shock liver) is the most common cause of acute liver injury, characterized by centrilobular liver cell necrosis and a sudden surge in serum aminotransferases (AST, ALT) resulting from cardiac, circulatory, or respiratory failure. Although the liver is protected against hypoxia by dual blood supply from the portal vein and hepatic artery alongside highly permeable sinusoids, heart failure (39-70%), sepsis (15-30%), and respiratory failure (15%) account for over 90% of cases. While generally subclinical, patients present critically with shock or symptoms of underlying heart failure like hepatomegaly. Laboratory findings show a rapid increase and subsequent decline in aminotransferases and LDH, where an ALT/LDH ratio below 1.5 and an INR above 2 indicate a poor prognosis. Biopsy is rarely required, and diagnosis is based on acute failure and aminotransferases exceeding 20 times the upper normal limit. Without specific treatment, management relies on correcting the underlying cause, yet the mortality rate remains high at 56%.
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