According to a previous US study [2], cirrhosis causes portal hypertension due to hepatic sinusoidal obstruction syndrome, perisinusoidal fibrosis and blocked portal circulation, thereby resulting in reduced and slow blood flow in the liver. At present, it has been confirmed that [3-5] PVT involves multiple factors, including hypercoagulable state, endothelial injury and slow portal vein blood flow. In this case, EVT might lead to mechanical injury of local vascular endothelium and activation of endogenous coagulation [6], in particular, endoscopic intravenous tissue glue injection into the stomach could cause histological changes in the portal vein [7], which might be one of the causes for subsequent thrombosis. In addition, ETV changed the hemodynamics of the portal vein. At present, studies [8-9] have shown that portal vein blood flow increases after ETV, accompanied by turbulence and pooling and portal vein pressure increases, which may increase the probability of portal vein thrombus formation and development. Both the 2019 Chinese Operation Guidelines for TIPS [10] and the 2021 North American Operation Guidelines for TIPS [11] pointed out that PVT was one of the surgical indications of TIPS. Nevertheless, the patient refused TIPS after PVT. Although anticoagulant therapy was given when portal vein pressure could not be effectively controlled, thrombosis was still progressively aggravated, resulting in CTPV. It can be predicted that PVT will aggravate portal hypertension, increase the risk of oesophagogastric variceal bleeding (EGVB), reduce intrahepatic portal perfusion and damage the compensatory function of the liver. If thrombosis involves the SMV and splenic vein, it may cause severe complications such as intestinal infarction and splenic infarction [10], which increases the risk of death in patients with cirrhosis [12] and the technical difficulty in liver transplantation [13]. Therefore, we will follow up and pay attention to the prognosis of this patient.

Factors including widening of portal vein diameter, deterioration of liver function and large blood flow in the portal collateral circulation have been considered risk factors of PVT [14-17]. Although the risk factors of PVT have been studied, some hemorheological indexes have been ignored. As an important organ of hemorheology, the liver synthesises plasma proteins, lipids and coagulation factors. Additionally, the liver also plays an important and decisive role in hemorheology [18]. Due to the low concentration of fibrinogen, albumin and other large proteins in the body, plasma viscosity is low ^[19]. Jang Bohyun et al. [20] reported that fibrinogen increased with the increase in the inflammatory response and other macromolecular proteins. Chaudhary A et al. [21] found that ETV could lead to fibrosis of the splenic vein, and local inflammation may increase the blood viscosity of the portal vein system. Harding DJ et al. [22] believed that after splenectomy, local vascular intima of the portal vein system was damaged, and an inflammatory reaction and platelet adhesion and aggregation occurred, which was likely to cause PVT or mesenteric thrombosis. In this case, fibrinogen and platelet counts after ETV were higher than those before surgery. We speculate that because patients with cirrhosis have adapted to low blood viscosity for a long time, local vascular intimal damage and inflammatory reaction will also occur in the portal vein system after ETV, accompanied by platelet adhesion and aggregation and increased blood viscosity, resulting in the formation and progression of the portal vein or mesenteric thrombus. This patient was treated with anticoagulant therapy after the detection of PVT, but the progression of thrombosis could not be avoided. We believe that blood viscosity is affected by the haematocrit, fibrinogen, albumin, erythrocyte deformation and aggregation and plasma viscosity. Moreover, in patients with cirrhosis whose portal hypertension cannot be effectively controlled and hemodynamics of the portal vein system cannot be changed, whether anticoagulant therapy alone can prevent the progression of PVT is worthy of further exploration.

In conclusion, based on clinical practice, it is common for cirrhotic patients to develop PVT after EVT. Therefore, further prospective studies are needed to confirm their correlation and to explore the effect of PVT after EVT on the prognosis of patients with cirrhosis.