University of Foggia, Italy
Dr. Vincenzo Neri was born in Bari, Italy, on 15th March, 1946, graduated on 1970 in Medicine and Surgery in the University of Bari. He is full Professor of General Surgery in the Medical School of the University of Foggia, Polyclinic. He is Director of the Residency School of General Surgery and Department of General Surgery. He was President of the Course of Degree of Medicine and Surgery, University of Foggia, in the years from 1996 to 2002. He was Director of Department of Surgical Sciences , University of Foggia in the years from 2002 to 2008. He obtained the certificate of “Maitrise Universitaire en Pedagogie des Sciences de la Santè” on the Universitè Paris – Nord Bobigny. He is author of more than 330 scientific paper edited on national and international journals and chapters of books. His research interest is hepatobiliopancreatic surgery. He is member of scientific societies : SIC, IHPBA,AISP,EASL,NESA,SLS.
Severe acute pancreatitis (SAP) is defined as associated with local and/or systemic complications. Development of persistent organs failure within 72 hours of symptoms onset and/or of infected pancreatic, peripancreatic complications allows the definition of the most severe forms, identified as critical or ESAP that are overlapping definitions. Critical forms (ESAP) are characterized by a short course, progressive multiple organ dysfunction syndrome (MODS), early hypoxemia, high CT severity index, increased incidence of pancreatic, peripancreatic necrosis, infection and ACS. Peripancreatic fluid collection suggests the anatomical clinical scenario of necrotizing acute pancreatitis. Intrahepatic fluid collection is a rare occurrence. We have treated two cases of intrahepatic fluid collection in two patients with acute biliary pancreatitis. Many systemic and/or chronic diseases can be connected with a greater incidence of acute pancreatitis : e.g. systemic lupus erythematous, Sjogren-Gongerot syndrome, sarcoidose, systemic vasculitis, antiphospholipides syndrome, metabolic diseases. The association of AP with the diabetes is in evidence : the risk of acute pancreatitis is raised by diabetes, but also of severe acute pancreatitis and early severe and critical forms. AP is a biphasic disease. In the first phase of the disease (1-2 weeks), pancreas pathological alteration (CT severity index), multi-organ dysfunction and compartment syndrome are in evidence as discriminating data between severe and critical forms. In a late phase of pancreatitis evolution the septic complication of pancreatic and peripancreatic necrotic fluid collections assumes a discriminating role. In summary there are critical or early severe acute pancreatitis characterized in the initial phase by SIRS with multi-organ dysfunction and equally severe forms in the late phase (3-4 weeks), after resolution or at least control of MODS which are instead characterized by septic complication of fluid-necrotic collections. The prolonged evolution of the disease can be increased by metabolic disease as diabetes. Intrahepatic fluid collection in the course of acute biliary pancreatitis is a rare occurrence. The therapeutic approach is the same as that for pancreatic and peripancreatic fluid collections. In case of infection, the patient undergoes percutaneous US/CT guided drainage. This therapeutic procedure can be added to the therapeutic program for necrotizing acute biliary pancreatitis together with ERCP/ES and videolaparocholecystectomy (VLC). Treatment of SAP and ESAP is now more conservative and less invasive than in the past : intensive care, prevention of intestinal failure and assure papillary patency in the first phase of the disease. In the later phase therapeutic procedure for fluid necrotic collections, is US/CT percutaneous catheter drainage.