RESUMEN
Sinus of Valsalva aneurysm is a rare defect that can present with fatal complications in case of rupture. Heart failure symptoms are common due to high fraction of the resultant shunt. Multimodality imaging and invasive hemodynamic assessment is essential for comprehensive evaluation of the defect and guiding surgical planning. We describe the case of a 40-year-old woman who presented with heart failure symptoms and was found to have ruptured sinus of Valsalva aneurysm on transthoracic echocardiogram. Cardiac computed tomography angiography further characterized the defect and the associated anomalies. Right heart catheterization assessed the hemodynamic significance of the left to right shunt. Intraoperative findings highlighted the associated congenital anomalies including supracristal ventricular septal defect. The use of intraoperative transesophageal echocardiography proved essential in detecting worsening of the right ventricular outflow track infundibular dynamic obstruction post repair thus delineating the importance of maintaining adequate cardiac preload. This case highlights a stepwise approach in the anatomical characterization of sinus of Valsalva aneurysm using multimodality imaging and the use of hemodynamic assessment and intraoperative imaging to guide surgical planning.
Asunto(s)
Aneurisma de la Aorta , Defectos del Tabique Interventricular , Seno Aórtico , Adulto , Aneurisma de la Aorta/diagnóstico por imagen , Aneurisma de la Aorta/cirugía , Ecocardiografía , Ecocardiografía Transesofágica , Femenino , Humanos , Seno Aórtico/diagnóstico por imagen , Seno Aórtico/cirugíaAsunto(s)
Perforación del Esófago/cirugía , Técnicas de Sutura , Accidentes de Tránsito , Medios de Contraste , Drenaje , Perforación del Esófago/diagnóstico por imagen , Perforación del Esófago/etiología , Humanos , Ligadura , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias , Tomografía Computarizada por Rayos XRESUMEN
INTRODUCTION: Splenic rupture after laparoscopic surgery is a very rare complication. In this study, we report a case of a splenic laceration that occurred during a laparoscopic gastrostomy tube placement. The theorized mechanism in this case was acute disruption of a peri-splenic hematoma. CASE REPORT: A 64-year-old African-American male presented after a motor vehicle accident with multiple injuries and was admitted to a surgical intensive care unit, where he declined from ICU days 6 through 11. The patient underwent tracheostomy and laparoscopic gastrostomy tube placement given his significant neurologic deficits. Intraoperatively, the patient developed hypotension, leading to the discovery of hemoperitoneum and necessitating an emergent open splenectomy. CONCLUSION: Splenic rupture following laparoscopic procedures is a very rare phenomenon. In this case, we believe the splenic rupture was secondary to an acute disruption of a previously hemostatic splenic hematoma involving the abdominal wall during creation of capnoperitoneum.
RESUMEN
BACKGROUND: The purpose of this study was to compare the outcomes of thoracic endovascular aortic repair (TEVAR) without and with left subclavian artery (LSA) revascularization using the Nationwide Inpatient Sample (NIS) database. METHODS: NIS records from 2005 to 2013 were retrospectively analyzed to identify patients undergoing TEVAR without and with LSA revascularization. Perioperative outcomes were compared between the two groups. The LSA revascularization group was further subdivided to compare perioperative outcomes if the revascularization was performed pre- or post-TEVAR or if the revascularization was performed open versus endovascular. Comparisons were examined using univariable analysis and multivariable logistic regression. Multivariable models were constructed using a forward selection approach with P < 0.05 required for model entry. Odds ratios are expressed per standard deviation change for continuous covariates. Continuous variables were compared between different groups using t-test, and categorical variables were compared using the chi-squared test. All statistical analyses were performed using R (cran.r-project.org). RESULTS: 7,773 TEVAR patients were included in this study. 6,411 (82.5%) were performed without and 1,362 (17.5%) with LSA revascularization. The rate of revascularization for LSA coverage during TEVAR doubled after the Society for Vascular Surgery Guidelines recommending revascularization were published in 2009. Groups were not significantly different in age (65.5 ± 15.8 and 66.1 ± 14.4 years old, respectively), gender, or race. Multivariable analysis showed that although rates of spinal cord ischemia and upper extremity ischemia were similar, perioperative cardiac complications (OR 1.5, 95% CI [1.2, 1.9], P = 0.025), stroke (OR 2.1, 95% CI [1.6, 2.8], P = 0.001), and pulmonary complications (OR 1.9, 95% CI [1.7, 2.3], P < 0.001) were significantly higher in the patients undergoing TEVAR with LSA revascularization than those without. Of the 1,362 patients with LSA revascularization, 1,251 (91.9%) were performed pre-TEVAR and 111 (8.1%) were performed post-TEVAR. Among the 1,251 patients with pre-TEVAR LSA revascularization, 583 had open surgery and 553 had stenting. In 115 patients, LSA revascularization was coded as both open and endovascular. Compared with pre-TEVAR revascularization, post-TEVAR revascularization was associated with higher risks of pulmonary complications and spinal cord ischemia. Endovascular LSA revascularization had lower pulmonary and stroke morbidity versus open LSA revascularization. The perioperative outcomes for the LSA revascularization subgroups are summarized. CONCLUSIONS: TEVAR with LSA revascularization is associated with significantly increased rates of perioperative stroke and cardiopulmonary complications. LSA revascularization before TEVAR, compared with post-TEVAR revascularization, had lower perioperative complications. In high-risk patients, endovascular LSA revascularization may be recommended over open surgery.
Asunto(s)
Aorta Torácica/cirugía , Aneurisma de la Aorta Torácica/cirugía , Implantación de Prótesis Vascular/métodos , Procedimientos Endovasculares/métodos , Arteria Subclavia/cirugía , Anciano , Anciano de 80 o más Años , Aorta Torácica/diagnóstico por imagen , Aorta Torácica/fisiopatología , Aneurisma de la Aorta Torácica/diagnóstico por imagen , Aneurisma de la Aorta Torácica/mortalidad , Aneurisma de la Aorta Torácica/fisiopatología , Implantación de Prótesis Vascular/efectos adversos , Implantación de Prótesis Vascular/mortalidad , Bases de Datos Factuales , Procedimientos Endovasculares/efectos adversos , Procedimientos Endovasculares/mortalidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias/mortalidad , Estudios Retrospectivos , Medición de Riesgo , Factores de Riesgo , Arteria Subclavia/diagnóstico por imagen , Arteria Subclavia/fisiopatología , Factores de Tiempo , Resultado del Tratamiento , Estados Unidos/epidemiologíaRESUMEN
Hyperglycemia-induced endothelial dysfunction is characterized by enhanced inflammatory cytokine and adhesion molecule expression, and endothelial-monocyte adhesion. The adapter molecule CIKS (connection to IKK and SAPK/JNK; also known as Act1 or TRAF3IP2) is an upstream regulator of NF-κB and AP-1, and plays a role in inflammation and injury. Here we show that high glucose (HG; 25mM vs. 5mM d-glucose)-induced endothelial-monocyte adhesion and inhibition of endothelial cell (EC) migration were both reversed by CIKS knockdown. In EC, HG induced CIKS mRNA and protein expression via DPI-inhibitable Nox4-dependent ROS generation. Further, HG induced CIKS transcription and enhanced CIKS promoter-dependent reporter gene activation via Nox4, ROS, AP-1 and C/EBP. Coimmunoprecipitation and immunoblotting revealed CIKS/IKKß/JNK physical association under basal conditions that was enhanced by HG treatment. Importantly, CIKS knockdown inhibited HG-induced (i) IKKß and JNK phosphorylation, (ii) p65 and c-Jun nuclear translocation, and (iii) NF-κB- and AP-1-dependent proinflammatory cytokine, chemokine, and adhesion molecule expression. Similar to HG, the deleterious metabolic products of chronic hyperglycemia, AGE-HSA, AOPPs-HSA and oxLDL, also induced CIKS-dependent endothelial dysfunction. Notably, aortas from streptozotocin-induced and the autoimmune type 1 diabetic NOD and Akita mice showed enhanced DPI-inhibitable ROS generation and CIKS expression. Since CIKS mediates high glucose-induced NF-κB and AP-1-dependent inflammatory signaling and endothelial dysfunction, targeting CIKS may delay progression of vascular diseases during diabetes mellitus and atherosclerosis.