الفهرس 
Applied anatomy of portal veinOnly 14 pages are availabe for public view
 |  | from | 134 |  |  |
| | | from | 134 | | |
Abstract
The portal vein is the vein of the gut that drains blood from the abdominal part of the gastrointestinal tract from the lower third of esophagus to halfway down the anal canal including spleen, pancreas and gall bladder( Dean, et al. 2000)
The term portal vein thrombosis (PVT) refers to the complete or partial obstruction of blood flow in the trunk of portal vein , due to the presence of a thrombus in the vassel lumen (Bayraktar and Harmanci ,2006).This includes its right and left intrahepatic branches. It may even extend to the splenic or superior mesenteric veins or towards the liver involving intra hepatic portal branches (Chawla,2009). from a pathophysiological point of view, PVT is a consequence of the so-called ‘Virchow’s triad’, which comprises venous stasis, endothelial injury, and hyper coagulopathy. For this reason, the underlying cause of PVT includes malignancy, chronic liver diseases, local inflammatory processes, systemic disorders including myeloproliferative disorders, and thrombophilia. In a high percentage of patients two or more risk factors are present (Pieri, et al. 2013). According to time of development, localization, pathophysiology and evaluation
PVT can be classified as follow:
• Acute or chronic.
• Extra or intrahepatic.
• Occlusive or non-occlusive.
• Progressive or self-resolving.
PVT onset can be acute or chronic. This is an particular distinction, which is sometimes difficult to apply in clinical practice; patients who develop symptoms, such as abdominal pain, nausea, and fever, within sixty days prior to hospital admission, might have an acute PVT development (Ponziani,et al. 2010)
PVT can be classified into four categories, depending on the extension (Groeschl,et al 2016)confined to the portal vein beyond the confluence of the splenic vein; extended to the superior mesenteric vein, but with patent mesenteric vessels; extended to the whole splanchnic venous system, but with large collaterals; or with only fine collaterals (Basit, et al 2015).This classification is useful to evaluate patient’s operability and clinical outcome. In fact, when thrombosis is extended to both portal and mesenteric veins, the risk of bowel ischemia is considerable and mortality high, despite a lower risk of variceal bleeding( Rajesh, et al .2015). Approximately 43% of patients with portal vein thrombosis are asymptomatic ,clinical presentation of PVT depends on the site, extent (partial or complete), chronicity(acute or chronic), and course (progressive or self-resolving) of thrombosis determine their clinical presentation as well as their complications in affected patients .While partial PVT is usually discovered incidentally by routine diagnostics and remains clinically silent, the complete occlusion of the vein (90–100% of the lumen) is associated with abdominal and/or lumbar pain characterized by sudden onset or progressive development over the course of a few days( Pieri, et al.2013).Acute and complete thrombosis is usually associated with intestinal congestion and occasionally with non-sanguineous diarrhea. In this case, a diffuse and homogeneous thickening of the intestinal wall may be present in imaging Studies.
The most serious complication is intestinal infarction with amorality of 20–60%, leading to extended resections with a high risk of postoperative complications. In contrast to intestinal congestion, infarction often presents with persistent pain, hematochezia, guarding, contracture, ascites, or multi organ failure with metabolic acidosis. In a usually urgently performed CT scan, the major findings can include hypo- or hyper attenuated wall thickening, dilatations, abnormal or absent wall enhancement, mesenteric stranding, ascites, pneumatosis, and portal venous gas . It is important to emphasize that this complication is usually found when the mesenteric veins are involved. Interestingly, in a retrospective analysis performed in patients with mesenteric vein thrombosis, a lack of performing CT studies was associated with an increased mortality ( Camacho, et al.2015).
The majority of complications of long-standing PVT are due to portal hypertension. Collateralization of the portal vein might lead to the development of the so-called portal cavernoma(Trebicka,et al.2014). However, Porto systemic shunting can also develop, since these cavernous collaterals may not sufficiently drain the portal blood flow, and portal pressure is not sufficiently decreased. This usually presents as de novo appearance and/or progression of gastric or esophageal varices and may be complicated by bleeding .Bleeding due to PVT occurs about 100 times more often in patients with cirrhosis.Imaging diagnosis of acute and chronic PVT can be readily made using noninvasive methods including ultrasound and Doppler ,CT and MRI magnetic resonance angiography (MRA), and traditional portography or splenoportography. (Quarrie et al,2008)also complications as VB can be diagnosed by upper GIT endoscopy.
The goal of treating acute PVT is to restore theobstructed veins, which will prevent intestinal infarction and portal hypertension. Correction of thecausal factors should be achieved as soon as possible (Primignani M et al. 2010). Most patients with PVT are treated with immediate anticoagulation therapy. This is most often performed via continuous intravenous heparin infusion, but some authors report using low molecular weight heparin. chronic treatment optionsinclude warfarin or low molecular weight heparin and new oral anticoagulants Initial treatment of PVT should consist of anticoagulation with heparin if the patient is not experiencing any active bleeding. Other more invasive treatment modalities used in the setting of PVT include trans jugular catheterization of occluded veins, local thrombolytic infusion directly into the area of thrombosis or into the superior mesenteric artery, the creation of a trans jugular Porto systemic shunt, stent implantation, and mechanical thrombectomy( Diab, et al,2013). Nonselective beta-blockers or endoscopic band ligation are recommended for the primary prophylaxis of VB(variceal bleeding) in medium and large varices in the latest Baveno consensus (de Franchis R; et al .2010). There is no indication for prophylactic portal decompression (either TIPS or surgical shunt) in asymptomatic varices. The emergency therapy of VB is primarily endoscopic , a successful primary hemostasis can be achieved in 80–90% . Emergency portal decompression (TIPS or surgical shunt) is seldom indicated as there is no survival advantage Nonetheless, a few groups report excellent outcomes for early TIPS or operative portocaval shunt procedures ,so these procedures should be kept in mind for salvage procedures in un stoppable bleeding(Khan S, et al. 2006)