Congenital pouch colon revisited

Congenital pouch colon: follow-up and functional results after definitive surgery

“…As also described in earlier reports [4,6,7], despite the very high nature of the associated anorectal malformation, the sacrum is usually normal in all subtypes of CPC and, surprisingly, even in those with a cloacal deformity. The sphincteric musculature and striated muscle complex are well developed, although the levator ani may be thinner than normal, perhaps as a consequence of the high pelvic location of the pouch and its terminal fistula [1,7].…”

“…The sphincteric musculature and striated muscle complex are well developed, although the levator ani may be thinner than normal, perhaps as a consequence of the high pelvic location of the pouch and its terminal fistula [1,7]. During abdomino-posterior sagittal anorectoplasty, it is easy to place the terminal bowel in the correct anatomical position, with a minimal risk of damage to the pelvic nerves.…”

“…In 7 patients (31.9%), all with type I/II CPC, the initial surgical procedure had consisted of subtotal excision of the pouch after division/ligation of its fistula with the genitourinary tract, tubular colorraphy (TC), and an end-colostomy [5][6][7][8]. A window colostomy of the pouch had been performed in another center on a child with type II CPC.…”

“…The severity of the condition varies from complete absence of normal colon, the distal ileum opening into the colonic pouch, to the presence of a nearly complete length of normal proximal colon, with only the rectum or rectosigmoid colon being affected [1]. A unique feature of CPC is that most large series describing this anomaly have been reported from centers in northern India [2][3][4][5][6][7].…”

Congenital pouch colon: an unusual histological finding

“…The embryogenesis of CPC is not fully understood; however, Trusler et al [14] attributed this condition to the absence of the hindgut with some malformation of the terminal portion of the mid-gut. Dickinson [15], Upadhyaya [16], and Chadha et al [17] proposed that a vascular compromise in the region of the hindgut during early intra-uterine development could account for pouch colon malformation.…”