Appendiceal intussusception is rare with an estimated incidence of 0.01%. Although it is infrequently encountered, the few documented cases of this entity have shown it may mimic or indicate an underlying neoplasm when evaluated with colonoscopy. With the abundant use of multi-detector CT and increased utility of CT colonography, awareness of the radiologic findings of this condition has become increasingly important. Appendiceal intussusception, while potentially pathologic in its own right, may mimic or even coexist with other pathologies, both malignant and benign. We present a case of adult appendiceal intussusception without a "lead point" that was successfully diagnosed by CT imaging.

Background Sinistral portal hypertension results from obstruction or stenosis of the splenic vein and is characterized by normal portal vein pressures and liver function tests. Gastrointestinal bleeding is the most common presentation and indication for treatment. Although sinistral portal hypertension-related chylous ascites is rare, several cases have described successful treatment with portal venous, rather than splenic venous, recanalization. Splenectomy is effective in the treatment of sinistral portal hypertension-related bleeding, although recent studies have evaluated splenic vein stenting and splenic arterial embolization as minimally-invasive treatment alternatives. Splenic vein stenting may be a viable option for other presentations of sinistral portal hypertension. Case presentation A 59-year-old gentleman with a history of necrotizing gallstone pancreatitis was referred to interventional radiology for management of recurrent chylous ascites. Analysis of ascites demonstrated a triglyceride level of 1294 mg/dL. Computed tomography revealed splenic and superior mesenteric venous stricture. The patient elected to undergo minimally invasive transhepatic portal venography, which confirmed the presence of splenic vein and superior mesenteric vein stenosis. Venography of the splenic vein showed reversal of portal venous flow, multiple collaterals, and a pressure gradient of 14 mmHg. Two 10 mm × 40 mm Cordis stents were placed, which decreased the pressure gradient to 7 mmHg and resolved the portosystemic collaterals. At 6 months follow-up, the patient had no recurrent episodes of ascites. Conclusion The current case highlights the successful treatment of sinistral portal hypertension-related intractable chylous ascites treated with transhepatic splenic vein stenting. Splenic venous stent patency rates of 92.9% at 12 months have been reported. Rebleeding rates of 7.1% for splenic vein stenting, 16% for splenectomy, and 47.8% for splenic arterial embolization have been reported in the treatment of sinistral portal hypertension-related gastrointestinal bleeding. The literature regarding splenic vein stenting for sinistral portal hypertension-related ascites is less robust. Technical and clinical success in the current case suggests that splenic vein recanalization may be a safe and viable option in other sinistral portal hypertension-related symptomatology. Level of Evidence: Level 4, Case Report.

Background: Sinistral portal hypertension results from obstruction or stenosis of the splenic vein and is characterized by normal portal vein pressures and liver function tests. Gastrointestinal bleeding is the most common presentation and indication for treatment. Although sinistral portal hypertension-related chylous ascites is rare, several cases have described successful treatment with portal venous, rather than splenic venous, recanalization. Splenectomy is effective in the treatment of sinistral portal hypertension-related bleeding, although recent studies have evaluated splenic vein stenting and splenic arterial embolization as minimally-invasive treatment alternatives. Splenic vein stenting may be a viable option for other presentations of sinistral portal hypertension. Case Presentation: A 59-year-old gentleman with a history of necrotizing gallstone pancreatitis was referred to interventional radiology for management of recurrent chylous ascites. Analysis of ascites demonstrated a triglyceride level of 1,294 mg/dL. Computed tomography revealed splenic and superior mesenteric venous stricture. The patient elected to undergo minimally invasive transhepatic portal venography, which confirmed the presence of splenic vein and superior mesenteric vein stenosis. Venography of the splenic vein showed reversal of portal venous flow, multiple collaterals, and a pressure gradient of 14 mmHg. Two 10 mm x 40 mm Cordis stents were placed, which decreased the pressure gradient to 7 mmHg, and resolved the portosystemic collaterals. At 6 months follow-up, the patient had no recurrent episodes of ascites. Conclusion: The current case highlights successful treatment of sinistral portal hypertension-related intractable chylous ascites treated with transhepatic splenic vein stenting. Splenic venous stent patency rates of 92.9% at twelve months have been reported. Rebleeding rates of 7.1% for splenic vein stenting, 16% for splenectomy, and 47.8% for splenic arterial embolization have been reported in the treatment of sinistral portal hypertension-related gastrointestinal bleeding. The literature regarding splenic vein stenting for sinistral portal hypertension-related ascites is less robust. Technical and clinical success in the current case suggests that splenic vein recanalization may be a safe and viable option in other sinistral portal hypertension-related symptomatology.Level of Evidence: Level 4, Case Report