Pathophysiology

It has been shown that the primary pathology in the causation of primary rectal ectasia is due to a deficiency in the smooth muscle causing weakening and dilatation of the rectal wall [17]. Secondary rectal ec-tasia develops due to the response to the obstructed rectum. The elasticity of the rectal wall permits the normal rectum to expand to approximately double the caliber, but it returns to its normal size. In the newborn, ectasia beyond this diameter is predictive of a primary developmental ectasia, which is made even more apparent when overdistended by gas and meconium content.

In the case of obstructive anorectal conditions, the rectal caliber soon reverts to normal dimensions after the relief of obstruction by surgery. If the rectal ampulla is developmentally ectatic, the dilatation may persist and lead postoperatively to fecal accumulation, further enlargement, troublesome constipation, and soiling.

With high rectal anomalies, the terminal bowel is frequently focally ectatic, and in many patients the ectasia is primary or developmental. In others, hypertrophy and dilatation may occur as reactions to propulsive activity against an obstruction or upon a retained meconium bolus in the terminus of the bowel after a defunctioning colostomy [23]. Primary and secondary rectal ectasia can be differentiated histologically by examining rectal specimens: hypertrophy and hyperplasia of smooth muscle cells is evident in acquired cases, and are normal or smaller in newborns with a primary or developmental anomaly. Dysplastic nitrergic neurons in the rectum of a patient with rectal ectasia have also been demonstrated [24]. Bowel activity after anorectal reconstruction for high lesions is compatible with near-normal continence in many children. Even when the sphincter muscles are adequate for high-grade continence, the ectatic terminal reservoir may overload and overflow, requiring long-term treatment.

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