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A 59-year-old man presented with recurrent upper gastrointestinal bleeding (UGIB) following an initial episode of gallstone pancreatitis in 2003. He underwent cholecystectomy but then had multiple hospital admissions for recurrent pancreatitis complicated by a large inflammatory pancreatic head mass in 2009. A Whipple’s procedure was attempted, but extensive adhesions to multiple vascular structures prevented safe resection of the pancreatic head mass and the procedure was converted to a roux-en-Y procedure. Ongoing inflammation and fibrosis surrounding the portal vein led to noncirrhotic portal hypertension complicated by large varices. These were first recognized in November 2011 when the patient presented with UGIB, treated with endoscopic variceal injection with N-butyl-2-cyanoacrylate (NBCA) (Histoacryl, Tuttlingen, Germany). The patient had multiple hospitalizations (8 admissions over a 22-month period) including an intensive care unit admission for lifethreatening UGIB secondary to both gastric and duodenal varices. These were managed medically with multiple blood transfusions (over 10 U in total), octreotide, and pantoprazole. Endoscopy was performed at each admission and therapy consisting of NBCA injections and variceal banding was performed when active UGIB was identified. Additionally, a suspicion of sinistral portal hypertension was treated with splenic debulking using staged partial particle embolization of the spleen followed by main splenic artery embolization. This was complicated by splenic abscess requiring splenectomy and distal pancreatectomy in 2012. In April 2013, further surgical management with a side-to-side portocaval shunt at the level of the porta hepatis was performed. No varices were ligated at the time of surgery. Despite these multiple treatments, the patient had two further episodes of UGIB requiring hospitalization. CT examination in June 2013 demonstrated a 2.8-cm long occlusion of the main portal vein at the level of the pancreatic head mass in addition to large gastric and duodenal varices (Fig. 1). Endovascular recanalization of the portal vein occlusion was now considered his best treatment option. Under conscious sedation with fentanyl (Sandoz, QC, Canada) and midazolam (Pharmaceutical Partners of & Mollie C. M. Ferris Mollie.Ferris@albertahealthservices.ca

Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen. A brief overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.