U Nitsche1, J Siveke, H Friess, J Kleeff. 1. Chirurgische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München, Ismaninger Str. 22, 81675, München, Deutschland.
Abstract
BACKGROUND: Benign and malignant pathologies of the pancreas can result in a relevant chronic disease burden. This is aggravated by morbidities resulting from surgical resections as well as from progression of the underlying condition. OBJECTIVE: The aim was to summarize the current evidence regarding epidemiology, pathophysiology, diagnosis and treatment of endocrine and exocrine pancreatic insufficiency, as well as of pancreatic pseudocysts. MATERIAL AND METHODS: A selective literature search was performed and a summary of the currently available data on the surgical sequelae after pancreatic resection is given. RESULTS: Reduction of healthy pancreatic parenchyma down to 10-15 % leads to exocrine insufficiency with malabsorption and gastrointestinal complaints. Orally substituted pancreatic enzymes are the therapy of choice. Loss of pancreatic islets and/or islet function leads to endocrine insufficiency and pancreoprivic diabetes mellitus. Inflammatory, traumatic and iatrogenic injuries of the pancreas can lead to pancreatic pseudocysts, which require endoscopic, interventional or surgical drainage if symptomatic. Finally, pancreatic surgery harbors the long-term risk of gastrointestinal anastomotic ulcers, bile duct stenosis, portal vein thrombosis and chronic pain syndrome. CONCLUSION: As the evidence is limited, an interdisciplinary and individually tailored approach for delayed pancreatic morbidity is recommended.
BACKGROUND: Benign and malignant pathologies of the pancreas can result in a relevant chronic disease burden. This is aggravated by morbidities resulting from surgical resections as well as from progression of the underlying condition. OBJECTIVE: The aim was to summarize the current evidence regarding epidemiology, pathophysiology, diagnosis and treatment of endocrine and exocrine pancreatic insufficiency, as well as of pancreatic pseudocysts. MATERIAL AND METHODS: A selective literature search was performed and a summary of the currently available data on the surgical sequelae after pancreatic resection is given. RESULTS: Reduction of healthy pancreatic parenchyma down to 10-15 % leads to exocrine insufficiency with malabsorption and gastrointestinal complaints. Orally substituted pancreatic enzymes are the therapy of choice. Loss of pancreatic islets and/or islet function leads to endocrine insufficiency and pancreoprivic diabetes mellitus. Inflammatory, traumatic and iatrogenic injuries of the pancreas can lead to pancreatic pseudocysts, which require endoscopic, interventional or surgical drainage if symptomatic. Finally, pancreatic surgery harbors the long-term risk of gastrointestinal anastomotic ulcers, bile duct stenosis, portal vein thrombosis and chronic pain syndrome. CONCLUSION: As the evidence is limited, an interdisciplinary and individually tailored approach for delayed pancreatic morbidity is recommended.
Authors: Hjalmar C van Santvoort; Marc G Besselink; Olaf J Bakker; H Sijbrand Hofker; Marja A Boermeester; Cornelis H Dejong; Harry van Goor; Alexander F Schaapherder; Casper H van Eijck; Thomas L Bollen; Bert van Ramshorst; Vincent B Nieuwenhuijs; Robin Timmer; Johan S Laméris; Philip M Kruyt; Eric R Manusama; Erwin van der Harst; George P van der Schelling; Tom Karsten; Eric J Hesselink; Cornelis J van Laarhoven; Camiel Rosman; Koop Bosscha; Ralph J de Wit; Alexander P Houdijk; Maarten S van Leeuwen; Erik Buskens; Hein G Gooszen Journal: N Engl J Med Date: 2010-04-22 Impact factor: 91.245