Samant Hrishikesh, Asafo-Agyei Kwabena O., Kimyaghalam Ali, Garfield Karen
Ochsner Multiorgan Transplant Center
MCG Augusta University
Portal vein thrombosis (PVT) is a narrowing or blocking of the portal vein by a blood clot. Thrombosis can develop in the main body of the portal vein or its intrahepatic branches and may even extend to the splenic or superior mesenteric veins. PVT frequently occurs with cirrhosis of the liver but may also occur without an associated liver disease like malignancy, abdominal sepsis, or pancreatitis. The extrahepatic portal venous obstruction terminology should be considered a separate entity that refers to developing portal cavernoma or collaterals around chronic portal vein thrombosis. The portal venous system, originating from the vitelline venous system, close to the umbilical venous system, from the fourth to the twelfth weeks of gestation, drains blood from the gastrointestinal tract (excluding the lower third of the rectum) and biliopancreatic apparatus, including the spleen, pancreas, and gallbladder, to the liver. The veins that drain the gastrointestinal organs parallel the major arteries that supply the foregut, midgut, and hindgut, including the celiac, superior mesenteric, and inferior mesenteric arteries, respectively. These veins eventually convene at the portal vein, forming a single venous inflow tract into the liver. The celiac vein drains the foregut structures, including the stomach, through the second part of the duodenum. The superior mesenteric vein drains the third part of the duodenum through the initial two-thirds of the transverse colon. The inferior mesenteric vein drains the remaining one-third of the transverse colon through the rectum. These veins comprehensively drain nutrients and toxins from the digestive intake and ultimately provide approximately 75% of the liver's blood supply, with the remaining blood coming from the hepatic artery—eventually draining into the hepatic veins and systemic circulation. The portal vein forms the confluence of the splenic and superior mesenteric veins, draining the spleen and small intestine, respectively. Portal vein occlusion with thrombosis formation typically occurs in 2 main groups of patients: patients with cirrhosis and patients with prothrombotic disorders. Acute PVT occurs with abrupt thrombotic portal vein occlusion. Portal vein thrombosis can result in complete or partial occlusion of the vein and consequent clot propagation into the mesenteric and splenic tributaries. Features of chronic PVT, such as collateral circulation (eg, cavernous portal transformation) or portal hypertension, have not developed in acute PVT. If the patient's knowledge of when the clot developed is unknown and the patient does not have features of chronic PVT, the PVT can be referred to as being "recent." Managing recent PVT is the same as managing acute PVT.
门静脉血栓形成（PVT）是指血凝块导致门静脉狭窄或阻塞。血栓形成可发生在门静脉主干或其肝内分支，甚至可延伸至脾静脉或肠系膜上静脉。PVT常与肝硬化同时发生，但也可能在无相关肝脏疾病的情况下出现，如恶性肿瘤、腹腔感染或胰腺炎。肝外门静脉阻塞这一术语应被视为一个单独的实体，指的是围绕慢性门静脉血栓形成而发展的门静脉海绵样变或侧支循环。门静脉系统起源于卵黄静脉系统，在妊娠第4至12周时靠近脐静脉系统，负责将胃肠道（不包括直肠下三分之一）以及胆胰器官（包括脾脏、胰腺和胆囊）的血液引流至肝脏。引流胃肠道器官的静脉与供应前肠、中肠和后肠的主要动脉并行，分别包括腹腔干、肠系膜上动脉和肠系膜下动脉。这些静脉最终汇聚于门静脉，形成单一的静脉流入肝脏的通道。腹腔干静脉通过十二指肠的第二部分引流包括胃在内的前肠结构。肠系膜上静脉通过横结肠的前三分之二引流十二指肠的第三部分。肠系膜下静脉通过直肠引流横结肠的后三分之一。这些静脉全面引流消化摄入物中的营养物质和毒素，最终为肝脏提供约75%的血液供应，其余血液来自肝动脉，最终流入肝静脉和体循环。门静脉由脾静脉和肠系膜上静脉汇合而成，分别引流脾脏和小肠。门静脉血栓形成导致的门静脉闭塞通常发生在两类主要患者中：肝硬化患者和易栓症患者。急性PVT发生时门静脉突然血栓形成阻塞。门静脉血栓形成可导致静脉完全或部分阻塞，并随之使血栓蔓延至肠系膜和脾的分支。慢性PVT的特征（如侧支循环，如门静脉海绵样变）或门静脉高压在急性PVT中尚未出现。如果患者血栓形成的时间未知且没有慢性PVT的特征，则该PVT可被称为“近期发生的PVT”。处理近期发生的PVT与处理急性PVT相同。
