Risk factors for surgical site infection in children.

OBJECTIVES: To assess the appropriateness of using the indices developed by the Study on the Efficacy of Nosocomial Infection Control (SENIC) and the National Nosocomial Infections Surveillance (NNIS) project to determine risk factors for surgical site infection (SSI) in children and, if not appropriate, to explore the factors related to SSI in children so these factors could be used in a risk index for pediatric patients. DESIGN: Cohort study during more than 4 years. SETTING: La Paz University Hospital, a national reference center that serves Health Area 5 of Madrid, Spain, which has approximately 500,000 inhabitants. PATIENTS: Convenience sample consisting of the 3,646 children admitted for surgery who had a postsurgical stay of more than 2 days. RESULTS: A model with 8 predictive factors (degree of surgical contamination; duration of surgery; type of surgery; use of a peripheral venous catheter, central venous catheter, or urinary catheter; number of diagnoses; and SSI exposition time) was created. Its relation to the SSI rate was better than that of the SENIC or NNIS indices. Its sensitivity, specificity, and area under the receiver-operating characteristic curve were higher than that of the SENIC index. CONCLUSIONS: The model that we created seems to be more adequate for predicting SSI and evaluating pediatric patients' intrinsic risk than the SENIC and NNIS indices.     

Invaginated vein graft as nerve conduit: An experimental study

Vein grafts have been used for nerve repair in experimental and clinical studies. However, some concerns about their collapsability and the presence of valves which could block axonal growth have been put forth. We propose a modification to eliminate these potential problems by turning the vein inside out, obtaining an “invaginated” vein graft. We performed an experimental study on 61 adult Wistar rats, divided into 3 groups: control (non-operated) (n = 11); immediate repair, with 3 subgroups: invaginated vein graft (n = 10), vein graft (n = 10), and nerve graft (n = 10); and delayed repair, with 2 subgroups: invaginated vein graft (n = 10) and nerve graft (n = 10). Delayed repair was performed 3 to 4 weeks following division of the nerve. Electromyographical (EMG) assessment was performed in all operated animals at 2, 4, and 6 months after immediate reconstruction, and at 1 and 4 months after delayed repair. At the end of the study, all nerves were excised and a morphometric analysis was performed. We conclude that vein grafts are as useful as nerve grafts in immediate and delayed nerve repair, as there were no significant functional or histologic differences. We found no significant differences between invaginated vein grafts and non-invaginated vein grafts. However, electrophysiological results were slightly superior in the former. Regenerated axons were small, grouped in minifascicles with thin myelin sheaths. The venous adventitia did not interfere with axonal growth. © 1994 Wiley-Liss, Inc.     

Loss of heterozygosity for distal markers on 22q in human gliomas.

Loss of constitutional heterozygosity as determined through the analysis of restriction-fragment-length polymorphism (RFLP) on tumoral and constitutional DNA has proven to be helpful to delimit the location of tumor-suppressor genes in the human genome. In malignant gliomas this approach indicates that chromosomes 9p, 10, 17p, and 22 may contain genes of this category involved in its origin and/or progression. Regarding chromosome 22, the data so far provided by molecular studies confirmed those previously reported by cytogenetic studies, suggesting the existence of a sub-group of malignant gliomas characterized by monosomy of this chromosome. However, the precise location of the putative glioma suppressor gene on chromosome 22 remains ambiguous. We have performed a combined cytogenetic and RFLP study on a series of 31 gliomas, looking for structural abnormalities of this chromosome. In 3 instances, terminal deletions of the long arm of chromosome 22 were observed by both methodologies, suggesting that the band q13 region distal to the D22S80 marker might be the critical domain non-randomly involved in tumor suppression of gliomas.