Portal vein thrombosis in liver cirrhosis

Ciroza je završni stadij progresivne jetrene fibroze obilježen poremećajem arhitekture jetrenog tkiva i formacijom regenerativnih čvorića. Jedna od njenin komplikacija je tromboza portalne vene, odnosno portalna venska tromboza (PVT) koja se definira kao prisutnost tromba u portalnoj veni ili njenim granama, sa ili bez širenja u gornju mezenteričnu ili lijenalnu venu. Može se klasificirati prema stupnju opstrukcije na parcijalnu i kompletnu, prema stupnju proširenosti s obzirom na zahvaćenost okolnih vena te prema trajanju na akutnu i kroničnu. Poznato je da prevalencija PVT u cirozi raste paralelno s ozbiljnošću jetrene bolesti i iznosi oko 1% u kompenziranom stadiju, oko 10% u akutnoj dekompenzaciji i 10-44% u slučaju razvoja HCC-a. Patogeneza PVT u cirozi jetre je vjerojatno multifaktorijalna i nastaje kao rezultat promjena različitih sastavnica Virchowljeve trijade: usporenog toga krvi, hiperkoagulabilnosti i oštećenja endotela. Akutnu PVT obilježava naglo stvaranje tromba u portalnoj veni koja dovodi do njene parcijalne ili kompletne opstrukcije. Klinička slika može biti asimptomatska ili može uključivati grčeve u trbuhu, dispeptične tegobe ili proljev ukoliko je tromb zahvatio gornju mezenteričnu venu. Zahvaćanjem distalnog dijela gornje mezenterične vene može nastati crijevna ishemija, crijevni infarkt i ileus. Nakon 3-5 tjedana od akutne PVT dolazi do stvaranja mreže venskih kolaterala, odnosno kavernoma koji je obilježje kronične PVT. Ona se može otkriti asimptomatski ili se može razviti portalna hipertenzija čije su komplikacije zajedno s portalnom kolangiopatijom glavna klinička manifestacija kronične PVT. Terapijske mogućnosti uključuju antikoagulantne lijekove i transjugularni intrahepatalni portosistemski shunt (TIPS). Za bolje poznavanje prevencije i prognoze PVT potrebne su dodatne prospektivne studije.Cirrhosis is a late stage of progressive liver fibrosis characterized by disruption of liver tissue architecture and the formation of regenerative nodules. One of its complications is portal vein thrombosis (PVT), which is defined by the formation of a thrombus within the main portal vein or its branches, with or without spreading to the superior mesenteric or splenic vein. PVT can be evaluated based on its degree into partial and complete, extension regarding the involvement of the surrounding veins and age into acute and chronic. The prevalence of PVT in cirrhosis is known to increase parallely with the severity of liver disease and is around 1% in the compensated phase, around 10% in acute decompensation, and 10-44% in the case of underlying HCC. The pathogenesis of PVT in liver cirrhosis is probably multifactorial and results from changes in various components of the Virchow triad: slow blood flow, hypercoagulability, and endothelial damage. Acute PVT is characterized by a sudden thrombus formation in the portal vein leading to its partial or complete obstruction. The clinical presentation may be asymptomatic or may include abdominal cramps, dyspepsia, or diarrhea if the thrombus has affected the superior mesenteric vein. Involvement of the distal part of the superior mesenteric vein can lead to intestinal ischemia, intestinal infarction and ileus. After 3-5 weeks following an episode of acute PVT, a network of venous collaterals is formed, i.e., cavernoma, which is a feature of chronic PVT. It may be asymptomatic or portal hypertension may develop. Complications of portal hypertension together with portal cholangiopathy represent the main clinical manifestations of chronic PVT. Therapeutic modalities include anticoagulants and transjugular intrahepatic portosystemic shunt (TIPS). Additional prospective studies are needed to better define the prevention and prognosis of PVT