Tratamiento endovascular de urgencia con endoprótesis de aneurisma roto disecado de aorta torácica: A propósito de un caso

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Abstract

Los aneurismas de aorta torácica son menos comunes que los aneurismas de aorta abdominal y pueden encontrarse en aorta ascendente, arco aórtico, aorta descendente o en una combinación de estos segmentos. De estos aneurismas el 30% al 40% se originan en la aorta torácica descendente. En los aneurismas de aorta torácica existe una debilidad estructural de la pared de la aorta, que conlleva una dilatación arterial progresiva con eventual ruptura o disección. Aproximadamente, 50% de los aneurismas de aorta torácica son ateroscleróticos y ocurren como resultado de remodelado arterial y dilatación o a raíz de un metabolismo anormal del colágeno. La mayoría de los aneurismas de aorta torácica se descubren por casualidad durante la evaluación de otros problemas médicos. La meta del tratamiento de los aneurismas de aorta torácica, es prevenir la muerte debido a su ruptura. El riesgo de ruptura de los no tratados oscila entre 46% a 74% y la tasa de mortalidad por su ruptura es extremadamente alta. Los aneurismas de gran tamaño, en especial aquellos mayores de 6 cm, son más susceptibles de rupturas que los aneurismas de menor tamaño. El tratamiento endovascular, inicialmente desarrollado para los aneurismas de aorta abdominal, se introdujo en 1992 como una alternativa menos invasiva al tratamiento de cirugía abierta para los aneurismas de la aorta torácica descendente. En la actualidad, el injerto de stent endovascular en la aorta descendente o endoprótesis, recibe mayor atención como alternativa al reparo quirúrgico de los aneurismas de aorta torácica.

Translated abstract

Thoracic aortic aneurysms are less common than abdominal aortic aneurysms and can be found in ascending aorta, aortic arch, descending aorta or in a combination of these segments. 30% to 40% of these aneurysms are originated in thoracic descending aorta. In thoracic aortic aneurysms there exists a structural wall weakness that leads to a progressive arterial dilation with eventual rupture or dissection. Approximately 50% of all thoracic aortic aneurysms are atherosclerotic and are the result of arterial restructure and dilation or are due to an abnormal collagen metabolism. Most thoracic aortic aneurysms are only found by chance during other medical problems evaluation. The goal of thoracic aortic aneurysms treatment is the prevention of death due to its rupture. Ruptured risk of untreated aneurysms oscillates between 46% and 74% and mortality rate due to its rupture is extremely high. Large aneurysms, especially when they are greater than 6 cm in diameter are more susceptible of ruptures than smaller aneurysms. Endovascular treatment, initially developed for abdominal aortic aneurysms, was introduced in 1992 as a less invasive alternative to open surgery treatment for descending thoracic aortic aneurysms. Endovascular stent or endoprosthesis is actually getting more attention as an alternative to surgical repair of thoracic aortic aneurysms.

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Most cited references 17

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Thoracoabdominal aneurysm repair: results with 337 operations performed over a 15-year interval.

Andrew Davison, Joseph M. Corey, David Dorer … (2002)

To review perioperative results and late survival after thoracoabdominal aneurysm repair (TAA), in particular to assess the impact over time of epidural cooling (EC) on spinal cord ischemic complications (SCI). A variety of operative approaches and protective adjuncts have been used in TAA to minimize the major complications of perioperative death and SCI. There is no consensus with respect to the optimal approach. From January 1987 to November 2001, 337 consecutive TAA repairs were performed by a single surgeon. Clinical features included prior aortic grafts in 97 (28.8%) and emergent operation in 82 (24.6%), including rupture in 46 (13.6%) and dissection in 63 (19%). Operative management consisted of a clamp/sew technique with adjuncts in 93%. EC (since July 1993) to prevent SCI was used in 194 (57.6%) repairs. Variables associated with the end points of operative mortality and postoperative SCI were assessed with the Fisher exact test and logistic regression; late survival was estimated with the Kaplan-Meier method. Operative mortality was 8.3% and was associated with nonelective operation, intraoperative hypotension, total transfusion requirement, and the postoperative complications of paraplegia, renal failure, and pulmonary insufficiency. Postoperative renal failure and transfusion requirement were independent correlates of mortality. SCI of any severity occurred in 38 of 334 (11.4%) operative survivors, with 22/38 (6.6% of cohort) sustaining total paraplegia. EC reduced the risk of SCI in patients with types I-III TAA (10.6% vs. 19.8%, =.04). Independent correlates of SCI over the entire study interval included types I/II TAA, rupture, cross-clamp duration, sacrifice of T9-L1 intercostal vessels, and intraoperative hypotension. Late survival rates at 2 and 5 years were 81.2 +/- 3% and 67.2 +/- 5%. EC has decreased the risk of SCI after TAA repair. Decreasing the substantial proportion (nearly 25%) of patients requiring nonelective operation will improve results. Late survival is equal to that after routine AAA repair, indicating that the considerable resource expenditure required for TAA repair is worthwhile.