RESUMEN
OBJECTIVE: To report the initial case of robotic-assisted level IV inferior vena cava (IVC) tumor thrombectomy, with the supra- and infradiaphragmatic caval segments managed purely by a robotic-assisted technique. METHODS: A 67-year-old female presented with a 5.3 × 2.4 cm right renal tumor and a level IV IVC tumor thrombus, 16.5 cm in length, extending 1.5 cm into the right atrium. Through a robotic trans-abdominal approach, the infrarenal and retrohepatic IVC, left renal vein and right kidney were secured. Using a robotic transthoracic approach, the thrombus was milked out of the right atrium. The intrapericardial caval segment was secured and the right atrium was excluded. No cardiopulmonary bypass was used. A cavotomy was made at the right renal vein os and the tumor thrombus was extracted en bloc in a retrograde manner under transesophageal echocardiographic visualization. RESULTS: Total operative time was 211 minutes, including robotic docking, with 90 minutes spent on taking down intraabdominal adhesions. Caval clamp time was 13 minutes. Estimated blood loss was 100 mL. Postoperatively, the patient developed atrial fibrillation with rapid ventricular rate (RVR) requiring diltiazem infusion (Clavien Grade II). Hospital stay was 5 days. There were no further complications. Pathology revealed an Angiomyolipoma and negative surgical margins. CONCLUSION: This is the initial report of a purely robotic-assisted level IV IVC tumor thrombectomy. We used this technique for an angiomyolipoma with tumor thrombus extending 1.5cm into the right atrium, managing both the supra- and infradiaphragmatic caval segments robotically. This report further extends the field of robotic surgery.
Asunto(s)
Procedimientos Quirúrgicos Robotizados , Trombectomía/métodos , Vena Cava Inferior , Trombosis de la Vena/cirugía , Anciano , Femenino , Humanos , Trombosis de la Vena/patologíaRESUMEN
Here we present the case of a patient that suffered a cardiac arrest due to pulmonary embolus. The patient was resuscitated using extracorporeal membrane oxygenation and treated with ultrasound-accelerated catheter-directed thrombolysis during support on extracorporeal membrane oxygenation, with an excellent outcome. This case demonstrates that the use of extracorporeal membrane oxygenation and ultrasound-accelerated catheter-directed thrombolysis can be highly effective for managing select patients with pulmonary embolus and cardiac arrest.
Asunto(s)
Cateterismo Periférico/métodos , Oxigenación por Membrana Extracorpórea/métodos , Paro Cardíaco/terapia , Heparina/administración & dosificación , Embolia Pulmonar/complicaciones , Terapia Trombolítica/métodos , Angiografía , Anticoagulantes/administración & dosificación , Arteria Femoral , Vena Femoral , Estudios de Seguimiento , Paro Cardíaco/diagnóstico por imagen , Paro Cardíaco/etiología , Humanos , Infusiones Intraarteriales , Masculino , Persona de Mediana Edad , Embolia Pulmonar/diagnóstico , Embolia Pulmonar/fisiopatología , Tomografía Computarizada por Rayos X , Ultrasonografía , Función Ventricular Derecha/fisiologíaRESUMEN
Stem cell therapy holds great promise for the replacement of damaged or dysfunctional myocardium. Nitric oxide (NO) has been shown to promote embryonic stem (ES) cell differentiation in other systems. We hypothesized that NO, through NO synthase gene transfer or exogenous NO exposure, would promote the differentiation of mouse ES cells into cardiomyocytes (CM). In our study, NO treatment increased both the number and the size of beating foci in embryoid body (EB) outgrowths. Within 2 weeks, 69% of the inducible NO synthase-transduced EB displayed spontaneously beating foci, as did 45% of the NO donor-treated EB, compared with only approximately 15% in controls. Cardiac-specific genes and protein expression were significantly increased in NO-treated ES. Electron microscopy and immunocytochemistry revealed that these NO-induced contracting cells exhibited characteristics consistent with CM. At day 7 in culture, troponin T was expressed in 45.6 +/- 20.6% of the NO-treated ES cells but in only 9.25 +/- 1.77% of control cells. Interestingly, 50.4 +/- 18.4% of NO-treated ES cells were troponin T-negative and annexin V-positive. This apoptotic phenotype was seen in <1% of the control ES cells. These data strongly support our hypothesis that mouse ES cells can be accelerated to differentiate into CM by NO treatment. NO may influence cardiac differentiation by both inducing a switch toward a cardiac phenotype and inducing apoptosis in cells not committed to cardiac differentiation.