RESUMEN
Prosthetic vascular graft infection is an uncommon yet serious condition. Traditional management has included debridement, excision of the infected graft, and revascularization as needed. We report on two cases in which limb viability was maintained by using endovascular native vessel recanalization after excision of infected prosthetic grafts. This approach was successful in maintaining adequate limb perfusion in both cases. Endovascular native vessel recanalization should be considered as an option to maintain limb viability after excision of infected prosthetic vascular grafts, especially when autogenous conduit is lacking or limitation of the extent of surgery is desirable.
Asunto(s)
Angioplastia de Balón/métodos , Implantación de Prótesis Vascular/efectos adversos , Isquemia/etiología , Extremidad Inferior/irrigación sanguínea , Infecciones Relacionadas con Prótesis/etiología , Anciano , Angiografía , Aorta , Remoción de Dispositivos/efectos adversos , Femenino , Arteria Femoral , Humanos , Recuperación del Miembro , Persona de Mediana Edad , Infecciones Relacionadas con Prótesis/terapia , Reperfusión , Resultado del TratamientoRESUMEN
OBJECTIVE: The purpose of this study was to determine the differences in outcome related to initial management of aortic endograft limb occlusion (ELO). METHODS: During a 7-year period, 823 endovascular aneurysm repairs (EVARs) resulted in 25 ELOs in 22 patients. The initial management and outcome of these ELOs were reviewed. Median follow-up after ELO was 24.2 +/- 16.8 months. RESULTS: Initial EVARs included both unsupported unibody (n = 5) and supported modular (n = 17) devices. ELO was significantly more common in the unsupported unibody graft design (P <.024) and with extension of the graft limb to the external iliac artery (P <.001). ELO was managed with an endovascular approach (EVA), including some combination of mechanical thrombectomy (n = 8), angioplasty with or without stenting (n = 8), and thrombolysis (n = 2) in 12 patients and bypass procedures (femoral-femoral bypass, n = 11; axillofemoral bypass, n = 1; and aortofemoral bypass, n = 1) in 13. At 12-month follow-up, freedom from secondary procedures with EVA was 80.2 +/- 17.7% versus 53.2 +/-17.1% with extra-anatomic bypass (EB) (P = NS). Secondary patency was 100% with EVA and 80.6 +/- 14.4% with EB (P = NS). Of the 12 EVAs, there was 1 (8.3%) perioperative mortality with EVA and none with EB. EB failure was directly attributed to donor limb occlusion in 4 of 6 EVAs (67%), and when this occurred it resulted in bilateral lower extremity ischemia. Amputation was required in 2 of 12 (16.7%) EBs versus none of the 12 EVAs (P = NS). EVA never resulted in graft dislodgement or endoleak but did identify an underlying treatable cause in 8 of 12 (67%). CONCLUSION: Both EVA and EB are acceptable management strategies for ELO. The potential risk of graft dislodgement was not observed with an EVA. If EB is employed, assessment of the donor limb and treatment of any underlying lesions is advisable in an attempt to minimize future donor limb occlusion.
Asunto(s)
Angioplastia , Aorta/cirugía , Arteria Axilar/cirugía , Prótesis Vascular/efectos adversos , Arteria Femoral/cirugía , Oclusión de Injerto Vascular/terapia , Aneurisma de la Aorta/cirugía , Estudios de Seguimiento , Oclusión de Injerto Vascular/etiología , Humanos , Estudios Retrospectivos , Stents , Trombectomía , Terapia Trombolítica , Resultado del TratamientoRESUMEN
Open surgical repair of retrohepatic inferior vena cava (IVC) injuries can be technically difficult, usually requiring extensive hepatic mobilization and associated with significant morbidity. We report a case of uncontrolled hemorrhage from the retrohepatic inferior vena cava (IVC), which occurred during attempted resection of a large retroperitoneal leiomyosarcoma, and was successfully managed using an endoluminal stent-graft. This case demonstrates that endoluminal grafts can be successfully applied to control life-threatening hemorrhage arising from lesions in the retrohepatic IVC that are otherwise extremely difficult or inaccessible to direct surgical repair.
Asunto(s)
Angioplastia , Pérdida de Sangre Quirúrgica , Implantación de Prótesis Vascular , Hemostasis Quirúrgica/métodos , Stents , Vena Cava Inferior/lesiones , Adulto , Femenino , Humanos , Vena Cava Inferior/cirugíaRESUMEN
OBJECTIVES: R136K is a mutation of fibroblast growth factor-1 (FGF-1) in which arginine replaces lysine at the primary thrombin cleavage site. This may be important in vivo in inducing endothelial cell (EC) migration and coverage of arterial injury sites by allowing R136K to be used in a fibrin glue delivery system, without thrombin-induced degradation, in the absence of heparin. The objectives of this study were to determine whether R136K, with and without heparin, can induce migration of EC and smooth muscle cells (SMC) through fibrin glue, and to compare these results with those of wild-type FGF-1; and to determine the resistance of R136K to thrombin-induced degradation versus FGF-1. METHODS: The dose-response migration through fibrin glue induced by wild-type FGF-1 and the R136K mutant in the presence and absence of heparin was tested with EC and SMC. Migration was tested with 50, 100, and 200 ng/mL of both FGF-1 and R136K, either with or without 5 U/mL of heparin. Migration of EC was also assessed after growth inhibition with mitomycin C. A novel modified Boyden chamber-type migration assay using fibrin glue on the upper surface of the chamber filter was used to test migration. The fluorescent marker calcein was used to identify those cells that had migrated through the fibrin glue and were embedded in the filter. Molecular degradation by thrombin was assessed with sodium dodecylsulfate polyacrylamide gel electrophoresis. RESULTS: For EC, R136K in the absence of heparin induced significantly more migration than did FGF-1 at 50 (P <.002), 100 (P <.0001), and 200 (P <.0001) ng/mL. In the presence of heparin, a chemotactic response of EC to cytokine was seen at all doses, with no significant difference between FGF-1 and R136K. A dose-dependent difference was noted in this group between the 100 and 200 ng/mL concentrations of cytokine (for FGF-1, P <.0001; for R136K, P <.0001). SMC showed no difference in migration with FGF-1, R136K, or negative control at any dose in the presence or absence of heparin. Gel electrophoresis demonstrated that R136K was more resistant to thrombin degradation than was FGF-1. CONCLUSION: Site-directed mutagenesis of FGF-1 to R136K enables induction of heparin-independent migration of EC through fibrin glue at an optimal concentration of 100 ng/mL. Neither FGF-1 nor R136K elicits SMC migration through fibrin glue. The ability of R136K to induce EC migration through fibrin glue in the absence of heparin may prove useful in vivo by inducing EC migration and coverage of arterial injury sites, thus potentially reducing thrombogenicity and intimal hyperplasia.
Asunto(s)
Endotelio Vascular/citología , Endotelio Vascular/efectos de los fármacos , Adhesivo de Tejido de Fibrina/administración & dosificación , Fibrinolíticos/administración & dosificación , Factor 1 de Crecimiento de Fibroblastos/administración & dosificación , Heparina/administración & dosificación , Adhesivos Tisulares/administración & dosificación , División Celular/efectos de los fármacos , Movimiento Celular/efectos de los fármacos , Citocinas/administración & dosificación , Relación Dosis-Respuesta a Droga , Humanos , Miocitos del Músculo Liso/citología , Miocitos del Músculo Liso/efectos de los fármacos , Trombina/efectos de los fármacos , Trombina/metabolismoRESUMEN
PURPOSE: The purpose of this study was to determine the outcome of nonoperative management (NOM) of asymptomatic high-grade (80% to 99%) carotid stenosis. METHODS: From April 1994 to December 2000, asymptomatic high-grade (80% to 99%) carotid stenosis was identified in 196 carotid arteries in 180 male veterans. Of the original number identified, 137 carotid endarterectomies (CEs) were performed in 123 patients (OP group) and 59 carotid arteries in 57 patients were managed nonoperatively (NOM group.) The NOM group was further subdivided into those patients who refused care (NOM-R group; n = 21; 36.8%) versus those who were not offered CE on the basis of comorbid conditions (NOM-C group; n = 36; 63.2%). Clinical follow-up was obtained to determine rates of neurologic events, patient survival, and progression to occlusion. RESULTS: During the follow-up period, a total of 13 ipsilateral neurologic events occurred: two amaurosis fugax (15.4%), two transient ischemic attacks (15.4%), and nine strokes (69.2%). The NOM-R group had a significantly lower ipsilateral neurologic event-free rate when compared with the OP group at both 18 months (81% +/- 9.8% versus 96% +/- 1.8%; P <.02) and 2 years (81% +/- 10.6% versus 95% +/- 2.1%; P <.04.) However, the NOM-C group and the OP group had no significant difference in their ipsilateral neurologic event-free rate out to 3 years (96% +/- 6.8% versus 95% +/- 2.7%). As would be expected, the NOM-C group had a much lower patient survival rate when compared with either the OP group (59% +/- 9.2% versus 84% +/- 3.6% at 2 years; P <.002) or the NOM-R group (59% +/- 9.2% versus 100% at 2 years; p <.0001). The cumulative patency rate of carotid arteries in the NOM group was 86% +/- 7.6% at 3 years. Progression to occlusion was associated with a neurologic event in two of five occurrences. No carotid artery progressed to occlusion in the OP froup. CONCLUSION: Although CE is the preferred treatment for asymptomatic high-grade carotid stenosis, NOM is an acceptable alternative in selected patients at high risk with diminished life expectancy.