Intraperitoneal mesh implantation for fascial dehiscence and open abdomen.

BACKGROUND: Postoperative fascial dehiscence and open abdomen are severe postoperative complications and are associated with surgical site infections, fistula, and hernia formation at long-term follow-up. This study was designed to investigate whether intraperitoneal implantation of a composite prosthetic mesh is feasible and safe. METHODS: A total of 114 patients with postoperative fascial dehiscence and open abdomen who had undergone surgery between 2001 and 2009 were analyzed retrospectively. Contaminated (wound class 3) or dirty wounds (wound class 4) were present in all patients. A polypropylene-based composite mesh was implanted intraperitoneally in 51 patients, and in 63 patients the abdominal wall was closed without mesh implantation. The primary endpoint was incidence of incisional hernia, and the incidence of enterocutaneous fistula was a secondary endpoint. RESULTS: The incidence of enterocutaneous fistulas after wound closure post-fascial dehiscence (13% vs. 6% without and with mesh, respectively) or post-open abdomen (22% vs. 28% without and with mesh, respectively) was not significantly different. The incidence of incisional hernia was significantly lower with mesh implantation compared with no-mesh implantation in both contaminated (4% vs. 28%; p = 0.025) and dirty abdominal cavities (5% vs. 34%; p = 0.01). CONCLUSIONS: Intra-abdominal contamination is not a contraindication for intra-abdominal mesh implantation. The incidence of enterocutaneous fistula is not elevated despite the presence of contamination. The rate of incisional hernias is significantly reduced after intraperitoneal mesh implantation for postoperative fascial dehiscence or open abdomen.

Blood modulates the kinetics of reactive oxygen release in pancreatic ischemia-reperfusion injury.

OBJECTIVES: Reason for the unsuccessful use of antioxidants in transplantation might be the unknown kinetics of reactive oxygen species (ROS) release. In this study, we compared the kinetics of ROS release from rat pancreata in the presence and absence of blood. METHODS: In vivo, ischemia-reperfusion injury (IRI) was induced in pancreata of male Wistar rats by occlusion of the arterial blood supply for 1 or 2 hours. In vitro, isolated pancreata were single-pass perfused with Krebs-Henseleit bicarbonate solution. Reactive oxygen species were quantified by electron spin resonance spectroscopy using CMH (1-hydroxy-3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine) as spin label. Thiols (glutathione), nicotinamide adenine dinucleotide phosphate-oxidase activity, myeloperoxidase activity, and adenosine triphosphate content were measured. RESULTS: During reperfusion, an increase in IRI-induced ROS in arterial blood was noted after 2 hours of warm ischemia. In sharp contrast, ROS release was immediate and short lived in blood-free perfused organs. The degree of tissue damage correlated with nicotinamide adenine dinucleotide phosphate-oxidase activity and adenosine triphosphate content. Antioxidative capacity of tissues was reduced. CONCLUSIONS: Electron spin resonance spectroscopy in conjunction with spin labels allows for the detection of ROS kinetics in pancreatic IRI. Reactive oxygen species kinetics are dependent on the length of the ischemic period and the presence or absence of blood.

Protective role of heme oxygenase-1 in pancreatic microcirculatory dysfunction after ischemia/reperfusion in rats.

OBJECTIVES: Microcirculatory derangements caused by ischemia and reperfusion (I/R) play a pivotal role in acute and graft pancreatitis. The inducible enzyme heme oxygenase 1 (HO-1) has been shown to decrease I/R injury by modulation of capillary perfusion in other organs. It was the aim of this study to evaluate the effect of HO-1 induction on pancreatic microcirculation after I/R. METHODS: Rats were randomized into 4 groups: (1) sham controls; (2) 1-hour ischemia and 2-hour reperfusion (I/R); (3) I/R + cobalt protoporphyrin (CoPP), an HO-1 inducer; and (4) I/R + CoPP + tin protoporphyrin, an HO inhibitor. Functional capillary density (FCD) and leukocyte endothelium interaction were analyzed using intravital microscopy during reperfusion. Expression of HO-1 mRNA, HO-1 protein, and HO activity were assessed by Northern blot, Western blot, and an HO activity assay. RESULTS: Functional capillary density decreased significantly in the I/R group as compared with sham controls. Cobalt protoporphyrin treatment increased FCD to control values. In contrast, HO inhibition in CoPP-pretreated animals lowered FCD and increased leukocyte endothelium interaction significantly. Cobalt protoporphyrin administration increased HO-1 mRNA, protein, and HO activity, whereas activity of the enzyme was reduced after injection of tin protoporphyrin. CONCLUSIONS: Heme oxygenase 1 plays a beneficial role in pancreatic microcirculatory derangements after I/R. This could be of therapeutic relevance after pancreas transplantation and other forms of postischemic pancreatitis.