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      Colonic Necrosis in a 4-Year-Old with Hyperlipidemic Acute Pancreatitis

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          Abstract

          Here we report the case of a 4-year-old male with severe acute pancreatitis due to hyperlipidemia, who presented with abdominal pain, metabolic abnormalities, and colonic necrosis. This colonic complication was secondary to the extension of a large peripancreatic fluid collection causing direct serosal autodigestion by pancreatic enzymes. Two weeks following the initial presentation, the peripancreatic fluid collection developed into a mature pancreatic pseudocyst, which was percutaneously drained. To our knowledge, this is the youngest documented pediatric case of colonic necrosis due to severe pancreatitis and the first descriptive pediatric case of a colonic complication due to hyperlipidemia-induced acute pancreatitis.

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          Issues in Hyperlipidemic Pancreatitis

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            Issues in hyperlipidemic pancreatitis.

            Hypertriglyceridemia (HTG) is a rare cause of pancreatitis. Pancreatitis secondary to HTG, presents typically as an episode of acute pancreatitis (AP) or recurrent AP, rarely as chronic pancreatitis. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is an identifiable risk factor. The typical clinical profile of hyperlipidemic pancreatitis (HLP) is a patient with a preexisting lipid abnormality along with the presence of a secondary factor (e.g., poorly controlled diabetes, alcohol use, or a medication) that can induce HTG. Less commonly, a patient with isolated hyperlipidemia (type V or I) without a precipitating factor presents with pancreatitis. Interestingly, serum pancreatic enzymes may be normal or only minimally elevated, even in the presence of severe pancreatitis diagnosed by imaging studies. The clinical course in HLP is not different from that of pancreatitis of other causes. Routine management of AP caused by hyperlipidemia should be similar to that of other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. Reduction of TG levels to well below 1,000 mg/dL effectively prevents further episodes of pancreatitis. The mainstay of treatment includes dietary restriction of fat and lipid-lowering medications (mainly fibric acid derivatives). Experiences with plasmapheresis, lipid pheresis, and extracorporeal lipid elimination are limited.
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              Colonic complications of severe acute pancreatitis.

              Colonic complications are rare in acute pancreatitis. Over the last 9 years at St. Mary's Hospital, London, UK, we have managed severe acute pancreatitis by intensive supportive therapy followed by sub-total pancreatic resection and/or debridement in those who fail to improve. Of the 22 patients who have undergone this form of surgery, nine were found to have colonic involvement in the form of either necrosis or perforation. In addition, one patient presenting at West Middlesex University Hospital, Isleworth, UK, had severe acute pancreatitis and almost total colonic necrosis as an unexpected finding at emergency laparotomy. These ten patients comprised seven men and three women of median age 59 years and with a median of four Ranson criteria. In seven patients, colonic involvement was discovered at the time of pancreatic surgery or laparotomy for pancreatitis and in the remainder it presented between 1 and 3 weeks later as either a faecal fistula (n = 2) or persistent abdominal sepsis (n = 1). The ascending colon was involved in one patient, the splenic flexure and descending colon in one, the transverse colon in three, the splenic flexure alone in four, and one patient had almost total colonic involvement. All patients underwent resection of the involved colon and exteriorization with either a proximal colostomy (n = 7) or ileostomy (n = 3) and a distal mucous fistula. Pathological examination of the resected colons revealed a spectrum of changes from pericolitis through to ischaemic necrosis suggesting at least two possible mechanisms. Six patients died from overwhelming sepsis between 1 day and 4 weeks (median 11 days) after colonic resection. Severe acute pancreatitis must be recognized as a cause of colonic ischaemia and necrosis; this complication is associated with a very poor prognosis despite surgical intervention.
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                Author and article information

                Journal
                Case Rep Pediatr
                Case Rep Pediatr
                CRIPE
                Case Reports in Pediatrics
                Hindawi Publishing Corporation
                2090-6803
                2090-6811
                2016
                27 January 2016
                : 2016
                : 9123163
                Affiliations
                1Department of Pediatrics, Section of Pediatric Gastroenterology, University of Chicago, Wyler Pavilion C-474, 5839 S. Maryland Avenue, MC 4065, Chicago, IL 60637, USA
                2Department of Pediatrics, Section of Pediatric Surgery, The University of Chicago Hospitals, 5841 S. Maryland Avenue, MC 4062, Chicago, IL 60637, USA
                Author notes

                Academic Editor: Daniel K. L. Cheuk

                Article
                10.1155/2016/9123163
                4748093
                26925282
                66ece984-0ebb-4b5b-92c1-3d9299720372
                Copyright © 2016 Tiffany J. Patton et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 August 2015
                : 17 December 2015
                : 30 December 2015
                Categories
                Case Report

                Pediatrics
                Pediatrics

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