The possible mechanisms by which vesicouterine fistulas occur following caesarean sections include undetected bladder injury during caesarean section, inadvertent placement of a suture through the bladder during the repair of the uterus and abnormal blood vessel connections following multiple caesarean sections.It may also present following use of obstetric forceps, manual placenta removal, external cephalic version, morbidly adherent placenta, surgical removal of fibroids, rupture of the uterus, perforation of the uterus and radiation therapy in the treatment of cervical cancer.Vesicouterine fistula can also occur as a birth defect in conjunction with vaginal atresia. Diagnosis
The diagnosis of a vesicouterine fistula is made by demonstrating an abnormal connection between the cavities of the bladder and uterus. It can be diagnosed using hysterosalpingography, hysterography, cystography, magnetic resonance imaging (MRI) and computerised tomography. MRI has been found to have 100% accuracy in the diagnosis of vesicouterine fistula. It is also less invasive than other modalities and is considered the gold standard for diagnosis. Treatment
The options of treatment include watchful waiting for spontaneous resolution of the fistula, use of medications that can stop menstrual periods such as oral contraceptive pills, progesterone and gonadotropin releasing hormone analogs. Surgery can be carried out through the vagina, bladder or peritoneum and can be done via laparoscopic or robotic surgery.Watchful waiting is the treatment of choice in case of small fistulas. The bladder is catheterised for a period of 4 to 8 weeks in order to allow spontaneous closure of the vesicouterine fistula.
It has been suggested that aphthous stomatitis is not a single entity, but rather a group of conditions with different causes. Multiple research studies have attempted to identify a causative organism, but aphthous stomatitis appears to be non-contagious, non-infectious, and not sexually transmissible. The mucosal destruction is thought to be the result of a T cell (T lymphocyte) mediated immune response which involves the generation of interleukins and tumor necrosis factor alpha (TNF-α). Mast cells and macrophages are also involved, secreting TNF-α along with the T cells. When early aphthous ulcers are biopsied, the histologic appearance shows a dense inflammatory infiltrate, 80% of which is made up of T cells. Persons with aphthous stomatitis also have circulating lymphocytes which react with peptides 91–105 of heat shock protein 65–60, and the ratio of CD4+ T cells to CD8+ T cells in the peripheral blood of individuals with aphthous stomatitis is decreased.Aphthous stomatitis has been associated with other autoimmune diseases, namely systemic lupus erythematosus, Behçets disease and inflammatory bowel diseases. However, common autoantibodies are not detected in most patients, and the condition tends to resolve spontaneously with advancing age rather than worsen. Evidence for the T cell-mediated mechanism of mucosal destruction is strong, but the exact triggers for this process are unknown and are thought to be multiple and varied from one person to the next. This suggests that there are a number of possible triggers, each of which is capable of producing the disease in different subgroups.