Repair of large midline incisional hernias with polypropylene mesh: Comparison of three operative techniques

Polypropylene mesh is widely used for the reconstruction of incisional hernias that cannot be closed primarily. Several techniques have been advocated to implant the mesh. The objective of this study was to evaluate, retrospectively, early and late results of three different techniques, onlay, inlay, and underlay. The records of 53 consecutive patients with a large midline incisional hernia — 25 women and 28 men, mean age 60.4 (range 28–94) — were reviewed. Polypropylene mesh was implanted using the onlay technique in 13 patients, inlay in 23 patients, and underlay in 17 patients. Either the greater omentum or a polyglactin mesh was interponated between the mesh and the viscera. The records of these 53 patients were reviewed with respect to: size and cause of the hernia, pre- and postoperative mortality and morbidity, with special attention to wound complications. Patients were invited to attend the outpatient clinic at least 12 months after implantation of the mesh for physical examination of the abdominal wall. Postoperative complications occurred in 14 (26.4%) patients. The onlay technique had significantly more complications, as compared to both other techniques. Reherniation occurred in 15 (28.3%) patients. The reherniation rate of the inlay technique was significantly higher than after the underlay technique (44% vs 12%, P=0.03) and tended to be higher than the onlay technique (44% vs 23%, P=0.22). Repair of large midline incisional hernias with the use of a polypropylene mesh carries a high risk of complications and has a high reherniation rate. The underlay technique seems to be the better technique.     

Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation

Previous studies documented the abnormal association of heme and heme proteins with the sickle RBC membrane. We have now examined RBC ghosts and inside-out membranes (IOM) for the presence of nonheme iron as detected by its formation of a colored complex with ferrozine. Sickle ghosts have 33.8 +/- 18.2 nmol nonheme iron/mg membrane protein, and sickle IOM have 4.3 +/- 3.0 nmol/mg. In contrast, normal RBC ghosts and IOM have no detectable nonheme iron. The combination of heme and nonheme iron in sickle IOM averages nine times the amount of membrane- associated iron in normal IOM. Kinetics of the ferrozine reaction show that some of this nonheme iron on IOM reacts slowly and is probably in the form of ferritin, but most (72% +/- 18%) reacts rapidly and is in the form of some other biologic chelate. The latter iron compartment is removed by deferoxamine and by treatment of IOM with phospholipase D, which suggests that it represents an abnormal association of iron with polar head groups of aminophospholipids. The biologic feasibility of such a chelate was demonstrated by using an admixture of iron with model liposomes. Even in the presence of tenfold excess adenosine diphosphate, iron partitions readily into phosphatidylserine liposomes; there is no detectable association with phosphatidylcholine liposomes. To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes. This is not due simply to a deficiency of vitamin E, and this is profoundly inhibited by deferoxamine. Thus, while thiol oxidation in sickle membranes previously was shown to correlate with heme iron, the present data suggest that lipid peroxidation is related to nonheme iron. In control studies, we did not find this pathologic association of nonferritin, nonheme iron with IOM prepared from sickle trait, high-reticulocyte, postsplenectomy, or iron-overloaded individuals. These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs.     

Use of glycosylated hemoglobin to identify diabetics at high risk for penile periprosthetic infections.

We report an 18-month prospective study of 90 patients undergoing penile prosthesis implantation to evaluate a possible cause-and-effect relationship between degree of diabetic control and the risk of infection complicating the operation. Long-term diabetic control was objectively evaluated by measurement of the glycosylated hemoglobin of the patient, which is known to provide an objective value for degree of control for the preceding 60 to 90 days. Of 90 patients 5 (5.5%) had a periprosthetic infection requiring explantation and all infections occurred in the 32 diabetics (36%) in the population (p less than 0.009). Of the 32 diabetics 13 (41.1%) were poorly controlled with time as demonstrated by a glycosylated hemoglobin level of greater than 11.5% and 4 of the infections occurred in this group. Of the 19 remaining controlled diabetics (glycosylated hemoglobin level less than 11.5%) only 1 infection occurred. Therefore, infection occurred in 31% of the poorly controlled versus 5% of the adequately controlled patients (p less than 0.0003). Measurement of glycosylated hemoglobin values appears to be a useful tool to evaluate diabetic patients before implantation of a penile prosthesis. Patients with a glycosylated hemoglobin level of 11.5% or greater should be more optimally controlled before undergoing implantation in an effort to avoid infectious complications.     

Is Serum the Optimal Source for HLA Antibodies?

The cytotoxic reactivity of 18 predefined class I HLA serum antibodies was compared with that of antibody preparations containing anticoagulants. ACD-A, EDTA, 4% citrate and heparin plasmas all showed lower cytotoxicity than serum antibodies. Recalcification of both platelet-rich and platelet-poor ACD-A plasma did not fully restore the antibody reactivity, suggesting a detrimental effect of calcium chelation. This effect was exclusive of volume or of any platelet or plasma protein involvement. The changes in pH contributed to the lower reactivity and to the increased lympholytic effect, whereas adjusting the pH toward the serum value improved the reactivity. Heat-inactivated antibodies showed only a slightly reduced cytotoxicity. Heparin had the least effect of all anticoagulants on the reactivity, although in heparin there was a definite dose-dependent decline in cytotoxic titer which was probably related to anticomplementary activity. Calcium chelators, such as EDTA and citrate, showed marked cytotoxic inhibition at half the usual complement concentration. This effect was more pronounced when the anticoagulant and lymphocytes were incubated prior to cytotoxicity testing. At the complement concentrations used, the inhibitory effects of the citrate anticoagulants appeared to be primarily calcium-related. Inhibition tests, serial titrations and testing of varying calcium concentrations confirmed the superiority of serum as antibody source.