Complications after pancreaticoduodenectomy: intraabdominal abscess RICHARD D. SCHULICK Departments of Surgery, Oncology, Biomedical Engineering, and Obstetrics and Gynecology, Johns Hopkins Medical Institutions, 1650 Orleans Street, Room 442, Baltimore, Maryland 21231, USA Offprint requests to: R.D. Schulick Received: September 20, 2007 / Accepted: October 20, 2007 Abstract The development of intraabdominal abscess (IAA) following pancreaticoduodenectomy (PD) is an important problem. It is a common cause of readmission to the hospital following discharge. Rates of IAA do not appear to depend on whether the pancreas is anastomosed to the stomach or jejunum, nor whether a duct-to-mucosa or invagination technique is used. Most surgeons favor the use of closed-suction drains after PD. The use of fibrin glue sealant does not appear to reduce the rate of IAA. The use of preoperative biliary stenting increases wound infection rates, but not IAA rates. The use of internal and external pancreatic duct stents with PD to prevent IAA have yielded mixed results. Key words Intraabdominal abscess · Pancreaticoduodenec- tomy · Complication Introduction Pancreaticoduodenectomy (PD) is considered a complex surgical procedure that is associated with a relatively high complication rate. It was first successfully per- formed early in the twentieth century, but was rarely performed before 1935, when Whipple published his classic paper in the Annals of Surgery. 1 Subsequently, because of hospital mortality in the range of 25%, PD was performed infrequently until the 1980s, at which time several institutions around the world became inter- ested in this operation. They started attracting large numbers of patients with both malignant and benign disease, and became regional centers of excellence. Institutions performing large volumes of this procedure started reporting their results, with substantially decreased hospital mortality; but morbidity, including postoperative pancreatic fistula, intraabdominal abscess (IAA), and delayed gastric emptying, remains a signifi- cant problem. 2–6 IAA following PD is most likely the consequence of pancreatic fistulae and/or leakage from the pancreatico- or hepatico-intestinal anastomosis. IAAs can also, rarely, be secondary to leakage from the duodeno- or gastrojejunostomy. They are often associated with increased morbidity and even mortality, secondary to sepsis. Intraabdominal fluid collections are common in the early postoperative period and should not be con- fused with the more serious finding of an abscess, which is manifested by signs of sepsis (fever, chills, malaise, increased abdominal pain, increased white blood cell count, and ileus). Often, benign postoperative fluid col- lections have thin walls and simple fluid density, and they do not have associated air on imaging. Postopera- tive IAAs, on the other hand, have thickened walls and complex fluid density, and they frequently have both air and fluid within the cavity. The treatment of choice for larger IAAs (typically greater than 4 or 5 cm) is drain- age by percutaneous catheter techniques, in which cath- eters can be placed under ultrasound or computed tomography guidance. Typically, patients benefit from a course of broadspectrum antibiotics that is tapered once the offending organisms are known. However, once the abscess is adequately drained and any ongoing leak well-controlled and the patient symptomatically improved, the antibiotics may be stopped. Smaller IAAs, especially (less than 4 cm) can be treated with antibiotics without drainage. This approach is typically used if the patient is not significantly ill and/or if the location of the abscess is difficult to approach safely with catheters. If patients do not respond adequately to these initial measures, surgical reintervention may be required for adequate drainage, peritoneal lavage, and placement of sufficient drains. In some circumstances, patients may require completion pancreatectomy, espe- cially if any ongoing pancreatic leakage is deemed life-threatening. J Hepatobiliary Pancreat Surg (2008) 15:252–256 DOI 10.1007/s00534-007-1302-x