Investigations for incontinence and constipation after surgery for Hirschsprung's disease in children

Investigations for incontinence and constipation after surgery for Hirschsprung's disease in children
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DOI:
10.1007/s00383-002-0897-x
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发表时间:
2003-04-01
影响因子:
1.8
通讯作者:
de Sousa, NM
de Sousa, NM
中科院分区:
医学3区
文献类型:
--
作者:
Keshtgar, AS;Ward, HC;de Sousa, NM

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先天性巨结肠症的手术与高发病率有关,表现为便秘或大小便失禁,或两者兼而有之。本研究探讨先天性巨结肠拉出术后大小便失禁和/或便秘的发生机制。有19名儿童(15名男孩和4名女孩),在研究期间;16名儿童接受了Duhamel,1名Rehbein和2名Soave手术。根据症状将患者分为3组:A组大便失禁,B组便秘大便失禁,C组单纯便秘。转诊时的中位年龄为6岁,术后中位年龄为5年。所有患者均进行了肠道传输检查、肛门内超声检查和肛门直肠测压。A组接受正常或快速转运研究,而B组和C组接受延迟转运研究。在肛门内超声检查中,所有儿童的内括约肌和外括约肌均完好无损,低于拔除手术的水平。肛门直肠测压显示,与B组或C组中有或无大小便失禁的便秘儿童相比,大小便失禁A组的静息肛压显著降低(分别为38毫米汞和57毫米汞和66毫米汞)。A组儿童的直肠压力也显著高于B组或C组(71毫米汞柱对42毫米汞或36毫米汞)。与B组或C组便秘患儿相比,A组大便失禁患儿的直肠/肛管压力比值较高。因此,便秘可由肛门静息压过高和直肠蠕动较弱引起,而在肛门括约肌静息压正常或过低的情况下,大便失禁可继发于顺应性差和直肠压力升高。大小便失禁是治疗便秘的主要手段,但大小便失禁儿童的治疗难度较大。我们没有尝试确定神经丛的类型,因为残存的神经节段和肠神经元发育不良的翻修手术效果不佳。如果提供详细的功能研究,这些儿童的治疗可以变得更加合理。我们主张对先天性巨结肠术后有症状的儿童进行早期肛门直肠功能调查,并在开始大手术前考虑较小的侵入性治疗。
Surgery for Hirschsprung's disease is associated with high rate of morbidity, in the form of either constipation or incontinence or a combination of the two. This study investigates the mechanisms responsible for incontinence and/or constipation following the pull-through operation for Hirschsprung's disease. There were 19 children (15 boys and 4 girls), who at the time of study; 16 had undergone Duhamel, 1 Rehbein, and 2 Soave operation. We classified patients according to their symptoms into 3 groups: Group A was incontinent of faeces; Group B was constipated and incontinent of faeces, and Group C was constipated only. The median age at referral was 6 years, and the median period after operation was 5 years. All patients were investigated by intestinal transit study, endoanal sonography and anorectal manometry. Group A had normal or rapid transit study, as opposed to Groups B and C, who had delayed-transit study. On endoanal sonography, all children had an intact internal and an external anal sphincter, bellow the level of pull-through operation. The anorectal manometry showed a significantly lower resting anal pressure in the incontinent Group A as compared to the constipated children with or without incontinence in Group B or C (38 mmHg versus 57 or 66 mmHg respectively). The rectal pressure was also significantly higher in children in Group A as compared to those in Group B or C (71 mmHg versus 42 or 36 mmHg). The ratio of rectal/anal pressure was higher in incontinent children in Group A, as compared to constipated children in Group B or C. Therefore, constipation can be caused by high anal resting pressure and a weak rectal peristalsis, while faecal incontinence can be secondary to poor compliance and elevated rectal pressure in the presence of normal or low anal sphincter resting pressure. Aperients are the mainstay of treatment of constipation, however, children with incontinence are more difficult to treat. We did not attempt to define the pattern of nerve plexus because of poor results of revision operation for residual hypoganglionic segment and intestinal neuronal dysplasia. Treatment of these children can become more rational, if furnished with detailed functional studies. We advocate investigation of the anorectal function at an early stage in symptomatic children after surgery for Hirschsprung's disease, and less invasive treatment should be considered before embarking on major surgery.