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1.
Langenbecks Arch Surg ; 407(7): 3089-3099, 2022 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-35906299

RESUMEN

PURPOSE: The use of synthetic mesh to repair infected abdominal wall defects remains controversial. Polyvinylidene fluoride (PVDF) mesh was introduced in 2002 as an alternative to polypropylene, with the advantages of improved biostability, lowered bending stiffness, and minimum tissue response. This study aimed to evaluate the short-term outcomes of using PVDF mesh to treat infected abdominal wall defects in the elective setting. METHODS: This prospective clinical trial started in 2016 and was designed to evaluate the short- and mid-term outcomes of 38 patients submitted to abdominal wall reconstruction in the setting of active mesh infection and/or enteric fistulas (AI) when compared to a group of 38 patients submitted to clean ventral hernia repairs (CC). Patients were submitted to single-staged repairs, using onlay PVDF mesh (DynaMesh®-CICAT) reinforcement to treat their defects. RESULTS: Groups had comparable demographic characteristics. The AI group had more previous abdominal operations and required a longer operative and anesthesia time. At 30 days, surgical site occurrences were observed in 16 (42.1%) AI vs. 17 (44.7%) CC, p = 0.817; surgical site infection occurred in 4 (10.5%) AI vs. 6 (15.8%) CC, p = 0.497; and a higher number of procedural interventions were required in the CC group, 15.8 AI vs. 28.9% CC, p = 0.169. Both groups did not have chronic infections at 1 year of follow-up, and one hernia recurrence was observed in the AI group. CONCLUSIONS: The use of PVDF mesh in the infected setting presented favorable results with a low incidence of wound infection.


Asunto(s)
Pared Abdominal , Hernia Ventral , Humanos , Mallas Quirúrgicas , Pared Abdominal/cirugía , Resultado del Tratamiento , Hernia Ventral/cirugía , Herniorrafia/efectos adversos , Herniorrafia/métodos , Recurrencia , Estudios Retrospectivos
2.
J Trauma ; 64(5): 1196-200; discussion 1200-1, 2008 May.
Artículo en Inglés | MEDLINE | ID: mdl-18469641

RESUMEN

BACKGROUND: Although the role of the lung alveolar macrophage (AM) as a mediator of acute lung injury (ALI) after lung ischemia/reperfusion (I/R) has been suggested by animal experiments, it has not been determined whether AMs mediate ALI after intestinal I/R. The objective of this study was to determine the effect of AM elimination on ALI after intestinal I/R in rats. METHODS: Male Wistar rats (n = 90) were randomly divided into three groups: the clodronate-liposomes (CLOD-LIP) group received intratracheal treatment with CLOD-LIP; the liposomes (LIP) group received intratracheal treatment with LIP; and the nontreated (UNTREAT) group received no treatment. Twenty-four hours later each group was randomly divided into three subgroups: the intestinal I/R subgroup was subjected to 45-minute intestinal ischemia and 2-hour reperfusion; the laparotomy (LAP) subgroup was subjected to LAP and sham procedures; the control (CTR) subgroup received no treatment. At the end of reperfusion, ALI was quantitated in all the animals by the Evans blue dye (EBD) method. RESULTS: ALI values are expressed as EBD lung leakage (microg EBD/g dry lung weight). EBD lung leakage values in the CLOD-LIP group were 32.59 +/- 12.74 for I/R, 27.74 +/- 7.99 for LAP, and 33.52 +/- 10.17 for CTR. In the LIP group, lung leakage values were 58.02 +/- 18.04 for I/R, 31.90 +/- 8.72 for LAP, and 27.17 +/- 11.48 for CTR. In the UNTREAT group, lung leakage values were 55.60 +/- 10.96 for I/R, 35.99 +/- 6.89 for LAP, and 30.83 +/- 8.41 for CTR. Within each group, LAP values did not differ from CTR values. However, in the LIP and UNTREAT groups, values for both the LAP and CTR subgroups were lower than values for the I/R subgroup (p < 0.001). The CLOD-LIP I/R subgroup value was less (p < 0.001) than the I/R subgroup values in the LIP and UNTREAT groups. These results indicated that I/R provokes ALI that can be prevented by CLOD-LIP treatment, and further suggested that AMs are essential for ALI occurrence induced by intestinal I/R in rats.


Asunto(s)
Conservadores de la Densidad Ósea/administración & dosificación , Ácido Clodrónico/administración & dosificación , Intestinos/irrigación sanguínea , Macrófagos Alveolares/efectos de los fármacos , Daño por Reperfusión/complicaciones , Síndrome de Dificultad Respiratoria/etiología , Animales , Permeabilidad Capilar , Liposomas , Macrófagos Alveolares/fisiología , Masculino , Fagocitosis , Ratas , Ratas Wistar , Síndrome de Dificultad Respiratoria/fisiopatología
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