Significant opportunities to advance educational research in this field exist by developing more high-quality studies with particular attention to randomization techniques and standardizing outcome measures.

Superior mesenteric artery (SMA) syndrome is a rare cause of small bowel obstruction (SBO) resulting from compression of the duodenum by the SMA. Patients at risk of developing SMA syndrome include those who have experienced rapid weight loss from chronic illnesses, malignancy, bariatric surgery, eating disorders, burns, trauma, or substance abuse. We present the case of a 54-year-old cachectic female patient who presented with sudden onset nausea, vomiting, and severe epigastric pain. Imaging studies revealed distention of the stomach and proximal portion of the duodenum with abrupt narrowing of the third part of the duodenum consistent with SMA syndrome. A laparoscopy confirmed the diagnosis and duodenojejunostomy resulted in resolution of the symptoms.

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INTRODUCTION: Polyarteritis Nodosa (PAN) is a rare systemic necrotizing vasculitis that preferentially affects medium-sized arteries. Patients may present with systemic symptoms or with isolated organ involvement. PAN may involve the gastrointestinal (GI), renal, cardiac, musculoskeletal, skin and central nervous systems. When the GI tract is involved, abdominal pain is the most common presentation, thought secondary to transmural necrotizing inflammation of the mesenteric vessels leading to bowel ischemia. The small bowel is the most common site of involvement. Ischemic mucosal ulceration, bowel infarction and perforation can result. Case reports in the pediatric literature and a retrospective case series have described PAN causing severe GI strictures leading to intestinal obstruction. We report a rare case of PAN leading to a colonic obstruction. CASE DESCRIPTION/METHODS: A 36-year-old-male was admitted to the hospital with nausea, vomiting, abdominal pain and reduction in the passage of stool and gas for the previous 5 months. Computerized topography of the abdomen and pelvis demonstrated colonic dilatation and obstruction at the level of the sigmoid colon. A flexible sigmoidoscopy was performed and identified severe stenosis at the recto-sigmoid junction, 25 cm from the anal verge. This area could not be traversed with an upper endoscope or an ultrathin endoscope. Given the near complete obstruction of the sigmoid colon, exploratory laparotomy was performed, which revealed a sigmoid stricture with densely adherent loops of small bowel. Sigmoidectomy with en bloc small bowel resection was performed. Pathology demonstrated mucosal ulceration with transmural inflammation and injury of the medium-sized vessels. Some of the medium-sized vessels in the mesentery had evidence of acute injury, while others appeared to be in the healing state with obliteration and recanalization of the lumen. This admixture of early and late lesions was felt consistent with PAN. The patient was discharged with GI, surgery and rheumatology follow up. DISCUSSION: PAN is a rare systemic vasculitis that can present with a wide range of symptoms including abdominal pain, nausea, vomiting, GI bleeding, diarrhea and weight loss. Intestinal stricture due to bowel ischemia can occur with resultant obstruction. The small intestine is the most common site of ischemia in the GI tract. As such the differential diagnosis of intestinal strictures should include chronic ischemia from systemic vasculitis.

INTRODUCTION: Hilar cholangiocarcinomas or Klatskin tumors (KT) pose significant diagnostic challenges; 15% of resections for KT prove to be non-malignant. Inflammatory, infectious, and other etiologies mimic radiological features of KT. A high index of suspicion is needed to avoid hepatic resection and associated morbidities while aggressively excluding KT. CASE DESCRIPTION/METHODS: A 64-year-old male who presented with jaundice, unintentional 50 lb weight loss, and fatigue was found to have bile duct dilation on ultrasound. A CT confirmed severe right and left hepatic duct dilatation with abrupt cutoff due to a 4 cm infiltrative hilar mass involving the right and left hepatic ducts, and extending into the common hepatic duct. Work-up for causes of jaundice (autoimmune hepatitis, hemochromatosis, alpha-1 antitrypsin deficiency, viral hepatitis, celiac sprue, autoimmune cholangiopathy) via ANA, AMA, F-actin, IgG, IgG4, HFE mutation, TIBC, ferritin, A1AT, tTG, hepatitis serologies was negative. Over 12 weeks, 3 ERCPs failed to confirm KT via biopsies, cytology, and fluorescence in situ hybridization (FISH). A severe proximal common hepatic duct stricture was found on initial ERCP, which was dilated and stented. ERCP with Spyscope showed hepatic bifurcation stricture improvement. This stricture was biopsied and again brushed, dilated and stented. A third ERCP showed further improvement in stricture and otherwise normal intra- and extra-hepatic ducts. Dilation to 8 mm was performed without further stenting. Cytology and FISH were negative for KT. Two CT guided biopsies of the mass were also negative for KT and failed to show biliary ductal thickening or clear evidence of the prior noted hilar mass. Two MRCPs, 7 months apart, showed significant improvement of right and left bile duct confluence stricturing, felt to represent fibrous tissue and scarring. DISCUSSION: Despite improvement in cross sectional imaging, advances in interventional radiologic and endoscopic modalities, differentiation between benign and malignant hilar biliary stenoses remains a major challenge. Up to 20% of hilar resection show chronic fibrosing inflammation without evidence of KT. We aggressively pursued this concern with 3 ERCPs (cytology, FISH, biopsy with Spyscope), and 2 CT guided biopsies. CT and MR showed radiologic improvement of the mass and lack of evidence of KT. Exclusion of autoimmune disease or other etiologies allowed a diagnosis of idiopathic inflammation, thus avoiding surgery.

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