

{"id":5787,"date":"2023-08-23T23:39:09","date_gmt":"2023-08-24T04:39:09","guid":{"rendered":"https:\/\/staging.advancedrenaleducation.com\/wparep\/?post_type=article&#038;p=5787"},"modified":"2025-05-09T11:05:28","modified_gmt":"2025-05-09T16:05:28","slug":"complicaciones-tardias-de-la-fistula-arteriovenosa-fav-estenosis-sp","status":"publish","type":"article","link":"https:\/\/staging.advancedrenaleducation.com\/wparep\/article\/complicaciones-tardias-de-la-fistula-arteriovenosa-fav-estenosis-sp\/","title":{"rendered":"Complicaciones tard\u00edas de la f\u00edstula arteriovenosa (FAV): Estenosis"},"content":{"rendered":"<p>La falla de la FAV puede discutirse en t\u00e9rminos de falla primaria (temprana) o falla tard\u00eda. Una revisi\u00f3n de la literatura actual revela variabilidad en la definici\u00f3n de falla primaria<sup>1<\/sup>; sin embargo, la falla tard\u00eda de la FAV se define con frecuencia como la falla que ocurre despu\u00e9s de tres meses de uso<sup>2<\/sup>. Las causas de la falla del acceso generalmente se pueden diagnosticar mediante im\u00e1genes mediante angiograf\u00eda o ecograf\u00eda d\u00faplex<sup>3,4<\/sup>. El uso de estas tecnolog\u00edas es importante porque la etiolog\u00eda de los problemas de acceso debe identificarse antes de que se puedan dise\u00f1ar las intervenciones adecuadas. Es importante darse cuenta de que las lesiones t\u00edpicas del fracaso temprano tambi\u00e9n se ven com\u00fanmente durante el per\u00edodo posterior, ya sea porque no se abordaron de manera oportuna o porque las lesiones han progresado y ahora son la fuente de disfunci\u00f3n<sup>2<\/sup>.<\/p>\n<p>La trombosis en el primer mes despu\u00e9s de la colocaci\u00f3n del acceso suele deberse a errores t\u00e9cnicos en la construcci\u00f3n de la f\u00edstula o en la selecci\u00f3n del vaso<sup>5<\/sup>. Las principales causas de trombosis f\u00edstula tard\u00eda incluyen estenosis venosa, compresi\u00f3n excesiva de la f\u00edstula posdi\u00e1lisis, hipotensi\u00f3n, compresi\u00f3n de la f\u00edstula debido a la posici\u00f3n para dormir, hipercoagulabilidad y ocasionalmente estenosis arterial<sup>5<\/sup>. La estenosis venosa es la causa m\u00e1s frecuente de p\u00e9rdida tard\u00eda de la FAV<sup>2,6<\/sup>. En un estudio, 63 f\u00edstulas maduras requirieron 209 procedimientos para mantener la permeabilidad<sup>2,7<\/sup>. El 83% (174\/209) de los procedimientos fueron angioplastia venosa para corregir la estenosis venosa<sup>2,7<\/sup>. Aunque no existe una definici\u00f3n coherente de estenosis, se ha utilizado un estrechamiento igual o superior al 50% de reducci\u00f3n del di\u00e1metro en comparaci\u00f3n con el vaso adyacente<sup>8<\/sup>.<\/p>\n<p>Aproximadamente el 50-60% de las estenosis se desarrollan en o cerca de la anastomosis arterial (yuxta-anastom\u00f3tica) de la f\u00edstula, mientras que el resto ocurre m\u00e1s proximalmente en la circulaci\u00f3n venosa, incluyendo hasta un 20% que involucra las venas centrales<sup>5,9<\/sup>. Las lesiones en la anastomosis arterial se desarrollan a partir de una hiperplasia progresiva de la neo\u00edntima (NH)<sup>9<\/sup>. Los mecanismos patog\u00e9nicos del NH incluyen la formaci\u00f3n por c\u00e9lulas de m\u00fasculo liso, fibroblastos y microvasos y modulaci\u00f3n de citocinas<sup>9,10<\/sup>. La patogenia del NH se inicia por lesi\u00f3n de las c\u00e9lulas endoteliales, posiblemente por flujo sangu\u00edneo turbulento, da\u00f1o vascular por angioplastia, calcificaci\u00f3n de fibrosis de v\u00e1lvulas venosas o trauma endotelial en ciertos puntos de presi\u00f3n anat\u00f3micos como el codo o la axila<sup>5,9<\/sup>.<\/p>\n<p>Las lesiones dentro de la f\u00edstula tambi\u00e9n pueden incluir co\u00e1gulos organizados en los sitios de canulaci\u00f3n frecuente; sin embargo, aproximadamente un tercio de la trombosis del acceso ocurre en ausencia de una lesi\u00f3n anat\u00f3mica<sup>5<\/sup>. La disminuci\u00f3n del flujo sangu\u00edneo de la f\u00edstula debido a un flujo de entrada inadecuado, la falta de dilataci\u00f3n adecuada, la hipotensi\u00f3n, la disminuci\u00f3n del gasto card\u00edaco, la hipovolemia o la compresi\u00f3n prolongada de la f\u00edstula durante el sue\u00f1o pueden contribuir a la trombosis en ausencia de una lesi\u00f3n anat\u00f3mica focal<sup>5,8<\/sup>. La trombosis de acceso no asociada a estenosis a menudo se debe a una compresi\u00f3n excesiva de la f\u00edstula para lograr la hemostasia despu\u00e9s de la di\u00e1lisis<sup>5<\/sup>. Se debe educar y capacitar al personal de di\u00e1lisis y a los pacientes para prevenir esta complicaci\u00f3n evitable.<\/p>\n<p>Aunque la estenosis es una complicaci\u00f3n indeseable de la FAV, las FAV tienen menos probabilidades que los injertos de desarrollar estenosis y trombosis<sup>11,12<\/sup>. En un estudio de 2004 de 543 fistulogramas (358 en injertos y 185 en f\u00edstulas), Maya et al determinaron que la probabilidad de encontrar una estenosis significativa era sustancialmente menor en las f\u00edstulas que en los injertos (39,4% versus 68,7% p &lt;0,001). Adem\u00e1s, entre los pacientes con estenosis significativa, aquellos con f\u00edstulas ten\u00edan menos probabilidades de tener 2 o m\u00e1s lesiones esten\u00f3ticas. (12,5% versus 33,1%; p &lt;0,001)<sup> 11<\/sup>. La permeabilidad a largo plazo de la FAV es superior a la de los injertos AV porque el riesgo de fallo secundario es mucho menor.<\/p>\n<div class=\"vcex-spacing\" style=\"height:30px\"><\/div><div class=\"vcex-module vcex-divider vcex-divider-solid\" style=\"width:100%;margin-top:20px;margin-bottom:20px;border-top-width:1px;border-color:#dddddd;\"><\/div>\n<h4>Referencias:<\/h4>\n<ol>\n<li>Ravani P, Spergel LM, Asif A, Roy-Chaudhury P, Besarab A. Clinical epidemiology of arteriovenous fistula in 2007. <em>J Nephrol<\/em>. 2007;20(2):141-149. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/17514618.<\/li>\n<li>MacRae JM, Dipchand C, Oliver M, et al. Arteriovenous Access Failure, Stenosis, and Thrombosis. <em>Can J kidney Heal Dis<\/em>. 2016;3:2054358116669126. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/28270918.<\/li>\n<li>Sands JJ, Ferrell LM, Perry MA. The role of color flow Doppler ultrasound in dialysis access. <em>Semin Nephrol<\/em>. 2002;22(3):195-201. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12012305.<\/li>\n<li>Malik J, Slavikova M, Malikova H, Maskova J. Many clinically silent access stenoses can be identified by ultrasonography. <em>J Nephrol<\/em>. 2002;15(6):661-665. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12495280.<\/li>\n<li>P Y Fan SJS. Vascular access: concepts for the 1990s &#8211; PubMed. J Am Soc Nephrol . Available from: https:\/\/pubmed.ncbi.nlm.nih.gov\/1391700\/.<\/li>\n<li>Roy-Chaudhury P, Spergel LM, Besarab A, Asif A, Ravani P. Biology of arteriovenous fistula failure. <em>J Nephrol<\/em>. 2007;20(2):150-163. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/17514619.<\/li>\n<li>Falk A. Maintenance and salvage of arteriovenous fistulas. <em>J Vasc Interv Radiol<\/em>. 2006;17(5):807-813. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16687746.<\/li>\n<li>Asif A, Gadalean FN, Merrill D, et al. Inflow stenosis in arteriovenous fistulas and grafts: a multicenter, prospective study. <em>Kidney Int<\/em>. 2005;67(5):1986-1992. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/15840048.<\/li>\n<li>Maya ID, Allon M. Vascular Access: Core Curriculum 2008. <em>Am J Kidney Dis<\/em>. 2008;51(4):702-708. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/18371547.<\/li>\n<li>Roy-Chaudhury P, Sukhatme VP, Cheung AK. Hemodialysis vascular access dysfunction: a cellular and molecular viewpoint. <em>J Am Soc Nephrol<\/em>. 2006;17(4):1112-1127. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16565259.<\/li>\n<li>Maya ID, Oser R, Saddekni S, Barker J, Allon M. Vascular access stenosis: comparison of arteriovenous grafts and fistulas. <em>Am J Kidney Dis<\/em>. 2004;44(5):859-865. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/15492952.<\/li>\n<li>Allon M, Robbin ML. Increasing arteriovenous fistulas in hemodialysis patients: Problems and solutions. <em>Kidney Int<\/em>. 2002;62(4):1109-1124. Available from: https:\/\/pubmed.ncbi.nlm.nih.gov\/12234281\/.<\/li>\n<\/ol>\n<p>P\/N 101048-01S Rev A 02\/2023<\/p>\n<div class=\"vcex-spacing\" style=\"height:30px\"><\/div>\n","protected":false},"featured_media":0,"template":"","format":"standard","meta":{"_acf_changed":false},"categories":[274],"tags":[181],"language":[42],"articles":[272],"class_list":["post-5787","article","type-article","status-publish","format-standard","hentry","category-articulos","tag-complications-sp","language-spanish","articles-hemodialisis","entry","no-media"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v26.2 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Complicaciones tard\u00edas de la f\u00edstula arteriovenosa (FAV): Estenosis - Advanced Renal Education Program<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/staging.advancedrenaleducation.com\/wparep\/article\/complicaciones-tardias-de-la-fistula-arteriovenosa-fav-estenosis-sp\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Complicaciones tard\u00edas de la f\u00edstula arteriovenosa (FAV): Estenosis - Advanced Renal Education Program\" \/>\n<meta property=\"og:description\" content=\"La falla de la FAV puede discutirse en t\u00e9rminos de falla primaria (temprana) o falla tard\u00eda. 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