Assuntos
Carcinoma Papilar/secundário , Exantema/diagnóstico , Neoplasias Renais/patologia , Neoplasias Cutâneas/secundário , Idoso , Carcinoma Papilar/diagnóstico , Carcinoma Papilar/terapia , Terapia Combinada , Diagnóstico Diferencial , Evolução Fatal , Humanos , Neoplasias Renais/terapia , Metástase Linfática , Masculino , Neoplasias Cutâneas/diagnóstico , Neoplasias Cutâneas/terapia , Tomografia Computadorizada por Raios XRESUMO
Suprapubic catheters are used routinely for bladder drainage; however, complications are commonly reported. These complications could be attributed to surgical technique or the catheter itself. Complications related to surgical technique can be controlled and reduced, but catheter-related complications are unavoidable and unpredictable. We report a rare catheter-related complication leading to obstruction of the ureter in a solitary kidney in a patient with neurogenic bladder and voiding dysfunction managed with suprapubic catheter drainage.
RESUMO
Hepatic transplantation may result in coagulopathy caused by the release of mast-cell-derived heparin, and xanthine oxidase (XO) inhibition stabilizes mast cells. Thus, XO inactivation could decrease coagulopathy after hepatoenteric ischemia-reperfusion. Rabbits were fed a standard or XO-inactivating diet before hepatoenteric ischemia for 35 min and before 30 min of reperfusion. Hemostasis was assessed by thrombelastography. Heparin activity was quantified by anti-IIa. XO inactivation resulted in clot formation after reperfusion in all animals, whereas only 37.5% of animals with XO activity clotted (P<0.05). Anti-IIa activity was less in animals at baseline and after reperfusion with XO inactivation (45+/-5 and 65+/-5 mU/mL, respectively) compared to animals with XO activity (51+/-4 and 71+/-5 mU/mL, respectively) (P<0.05). Clot strength, which was mediated by coagulation proteins, was significantly greater at baseline and after reperfusion in animals with XO inactivation. XO inactivation enhances hemostasis by decreasing circulating heparin activity and increasing coagulation protein function before ischemia-reperfusion.