Coagulation disorders in patients with liver cirrhosis

Ciroza je posljednji stadij kronične bolesti jetre, a poremećaji hemostaze koji nastaju u sklopu ovog stanja posljedica su smanjene sintetske funkcije jetre te portalne hipertenzije. U cirozi jetre snižene su koncentracije svih čimbenika zgrušavanja krvi i endogenih antikoagulansa uz iznimku faktora VIII koji se može naći u povišenim koncentracijama. Uspostavljena nova ravnoteža koja nastaje zbog relativnog manjka i čimbenika zgrušavanja krvi i prirodnih antikoagulansa u cirozi nije stabilna kao u fiziološkim uvjetima. Vrlo lako može doći do pomaka ravnoteže na stranu krvarenja ili tromboze, a što će prevagnuti ovisi o prisutnim rizičnim čimbenicima u pojedinog bolesnika (portalna hipertenzija, bakterijske infekcije, disfunkcija endotela, bubrežno zatajenje, uremija, varikoziteti jednjaka). Standardni testovi zgrušavanja krvi dobro koreliraju s težinom bolesti i mogu se koristiti za procjenu prognoze, no nažalost ne prikazuju dobro promjene u čitavom sustavu zgrušavanja krvi te ne mogu dobro procijeniti rizik za pojavu krvarenja ili tromboze u ove skupine pacijenata. Globalni viskoelastični testovi, poput tromboelastografije i rotacijske tromboelastometrije, omogućuju bolju procjenu sustava zgrušavanja krvi te se danas sve više koriste. Najčešća krvarenja su iz varikoziteta jednjaka te se smatraju posljedicom lokalnih promjena u području varikoziteta i portalne hipertenzije, a manje posljedicom samog poremećaja sustava zgrušavanja krvi. S druge strane portalna venska tromboza najčešći je trombotski događaj u pacijenata s cirozom jetre, a spori protok krvi u portalnom sustavu najznačajniji je čimbenik koji pridonosi riziku za trombozu. Odluke o terapijskim intervencijama potrebno je donositi individualno za svakog pacijenta, a često i u suradnji s hematologom.Liver cirrhosis presents an end stage of chronic liver disease and associated alterations in hemostasis result from an impaired synthetic function of the liver and portal hypertension. In cirrhosis levels of both procoagulants and anticoagulants are decreased, except for factor VIII which is increased. Consequently, the hemostasis in cirrhosis is rebalanced, because there is a relative deficit on both sides of the coagulation system, but this balance between the procoagulants and anticoagulants is not as stable as in physiological conditions. It can easily tip toward hemorrhage or thrombosis depending on the risk factors in each patient individually (portal hypertension, bacterial infections, endothelial dysfunction, renal failure, uremia, esophageal varices). Conventional coagulation tests are in good correlation with the severity of the disease and can be used as predicting factors, but they do not reflect all changes in the entire coagulation system and can not accurately predict the risk of bleeding or thrombosis in patients with liver cirrhosis. Global viscoelastic tests, such as thromboelastography and rotational thromboelastometry, enable better assessment of hemostatic balance and are being introduced into clinical practice. The most common bleeding event in patients with cirrhosis represents bleeding from ruptured esophageal varices, which develops as consequence of local vascular abnormalities as well as portal hypertension, while changes in hemostasis play a minor role in variceal bleeding. On the other hand, portal vein thrombosis is the most common thrombotic event in patients with liver cirrhosis and reduced portal blood flow represents the most important risk factor for portal vein thrombosis. Decisions on therapeutic interventions should be made individually for each patient and often in consultation with the hematologist