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Acute pancreatitis is described as two or more of the following criteria: abdominal pain suggestive of pancreatitis, serum amylase or lipase level greater than three times the upper limit of normal and characteristic imaging findings (1). Mild acute pancreatitis, or interstitial pancreatitis, is characterized by absence of organ failure or systemic complications. Moderately severe acute pancreatitis is characterized by transient organ failure (resolving within 48 hours) and/or local systemic complications without persistent organ failure (>48 hours). Severe acute pancreatitis is characterized by persistent organ failure that may involve one or more organ systems. This includes shock (systolic blood pressure <90 mmHg), pulmonary insufficiency (PaO 2 ≤60 mmHg), acute kidney injury (serum creatinine level >2 mg/dL), and gastrointestinal bleeding. Approximately 15-25% of all patients with acute pancreatitis develop severe pancreatitis with local complications, such as necrosis, pseudocyst, or abscess formation (2). NutritionPatients who develop pancreatitis are often placed NPO until the inflammation has resolved and can withstand an oral diet. Current ligature supports the notion that enteral nutrition is superior to parenteral nutrition. In severe acute

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shock (systolic blood pressure <90 mmHg), pulmonary insufficiency (PaO 2 ≤60 mmHg), acute kidney injury (serum creatinine level >2 mg/dL), and gastrointestinal bleeding. Approximately 15-25% of all patients with acute pancreatitis develop severe pancreatitis with local complications, such as necrosis, pseudocyst, or abscess formation (2). NutritionPatients who develop pancreatitis are often placed NPO until the inflammation has resolved and can withstand an oral diet. Current ligature supports the notion that enteral nutrition is superior to parenteral nutrition. In severe acute

Portomesenteric venous thrombosis is a rare complication reported in only a few cases involving laparoscopic bariatric surgery. We report a case of a 44-year-old woman who presented 14 days after recent laparoscopic sleeve gastrectomy with the chief complaint of abdominal pain and associated nausea. Abdominal CT demonstrated thrombi in her superior mesenteric, portal and splenic veins. She was initiated on therapeutic heparin but developed haemorrhagic shock shortly afterwards. Subsequent CT angiogram failed to localise the source of her haemorrhage. Her haemodynamic instability improved following a 6-day intensive care unit stay requiring vasopressive agents and blood transfusions. Further hypercoagulable workup revealed that she was a heterozygous carrier of the prothrombin gene mutation, and thus started on lifelong oral anticoagulation.