Article

Obstetric vesicovaginal fistula as an international public-health problem.

Department of Obstetrics-Gynecology, Washington University School of Medicine, St Louis, MO 63110, USA.
The Lancet (Impact Factor: 39.21). 10/2006; 368(9542):1201-9. DOI: 10.1016/S0140-6736(06)69476-2
Source: PubMed

ABSTRACT Vesicovaginal fistula is a devastating injury in which an abnormal opening forms between a woman's bladder and vagina, resulting in urinary incontinence. This condition is rare in developed countries, but in developing countries it is a common complication of childbirth resulting from prolonged obstructed labour. Estimates suggest that at least 3 million women in poor countries have unrepaired vesicovaginal fistulas, and that 30 000-130 000 new cases develop each year in Africa alone. The general public and the world medical community remain largely unaware of this problem. In this article I review the pathophysiology of vesicovaginal fistula in obstructed labour and describe the effect of this condition on the lives of women in developing countries. Policy recommendations to combat this problem include enhancing public awareness, raising the priority of women's reproductive health for developing countries and aid agencies, expanding access to emergency obstetric services, and creation of fistula repair centres.

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    ABSTRACT: In September, 2005, a 26-year-old woman came to our clinic, having been leaking urine constantly for 2 years. She had lived in rural Gambia, until migrating to Germany in July, 2005. She had given birth 3 years before she started to leak urine; the birth had been uncomplicated. She recalled no injury or surgery to the urinary tract or genitals. Examination, with a speculum, revealed a defect in the anterior vaginal wall, 3 cm from the introitus, through which urine was passing. Transvaginal ultrasonography showed no abnormality, except that the bladder could not be fi lled. Cystoscopy showed the fi stula to open into the bladder. Near the opening of the fi stula, we saw two blisters, nearly 1 cm in diameter. The blisters were yellow and fi ne-grained in appearance, rather like sand. We took biopsy samples from the blisters: histopathological examination showed eggs of Schistosoma haematobium, surrounded by chronic granulomatous infl ammation (fi gure). Cystography with contrast, and CT with contrast, showed the path of the fi stula; CT also showed the posterior wall of the bladder to be irregular, consistent with scarring from schistosomiasis. Blood tests showed eosinophilia, and a high concentration of IgE (2990 IU/mL; normal range ≤100 IU/mL). Dipstick testing of urine showed microhaematuria and proteinuria. Microscopy of a fresh urine sample obtained at noon, and passed through a nucleopore fi lter, revealed eggs of S haematobium, in which the larvae moved spontaneously, indicating that the eggs were viable. An indirect immunofl uorescence test showed antibodies to soluble egg antigen of Schistosoma spp, at a titre of 1:320. We tested for other infections by microscopy, culture, and PCR of urine and vaginal fl uid; many stool examinations; fi ltration of blood through nucleopore fi lters, after administration of diethylcarbamazine, which encourages fi larial larvae to move into the blood; and serological testing. However, we found no infections apart from schistosomiasis—and specifi cally, no evidence of chlamydia, syphilis, cytomegalovirus, HIV, human T-cell leukaemia virus, hepatitis B, hepatitis C, lymphatic fi lariasis, amoebiasis, or tuberculosis. We prescribed praziquantel, at a dose of 40 mg/kg, for 3 days. 8 weeks later, examination of a 24 h urine specimen showed no eggs of schistosoma; cystoscopy showed no blisters, although some sandy patches and cystitis cystica persisted. The fi stula opening was smaller than before. Histopathological examination of a biopsy sample from the sandy patches revealed a single, non-viable, egg of schistosoma. Since the patient continued to leak urine, we inserted a permanent catheter, but removed it 10 days later, because the patient found it uncomfortable. 4 months later, cystoscopy showed no mucosal abnormalities; moreover, the fi stula was very small indeed. The patient preferred surgery to further conservative treatment. She recovered well from the operation. When last seen, in March, 2008, she was well, and fully continent of urine. At least 3 million women are thought to have an untreated vesicovaginal fi stula (VVF). 1 VVF are usually attributed to injuries sustained during childbirth, or female genital mutilation 1 —although they can also be caused by infections. Schistosomiasis often aff ects the reproductive tract, 2,3 and was suspected, as long ago as 1907, to cause VVF. 4 However, it has not been established as a sole cause of VVF, since patients with schistosomiasis have tended to have other possible causes of VVF. 5 We were unable to identify any other cause of VVF in our patient, indicating that perhaps, after all, schistosomiasis can be a sole cause of VVF. Treatment of the disease coincided with regression of the fi stula. Schistosomiasis should always be treated before a fi stula is resected;
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