Primary rectal ectasia. A quantitative study of smooth muscle cells in normal and hypertrophied human bowel

The quantitative study showed that, in the normal human colon, smooth muscle cells increased both in size and in number in the first three years of life. Then the cell size remained relatively constant, having an anverage value of 4,260 cubic microns, while the cell number increased further with age. In the secondary megacolon in children with Hirschsprung's disease, both hypertrophy and hyperplasia of smooth muscle cells were found as a response to the obstruction. Release of obstruction by a defunctioning colostomy was followed by a reduction in size of the hypertrophied smooth muscle cells, but the increased cell number persisted for more than three months. The specimens of megarectum and megasigmoid colon associated with congenital rectal fistulae were different in their muscle cell dimensions according to the age after birth when the quantitation was undertaken. When examined weeks or months after birth, the walls of the enlarged viscus were thick, the muscle cells were hypertrophic and the numbers were greater than normal. Faecal masses, when present in the defunctioned obstructed bowel, probably induce hypertrophy and hyperplasia of muscle cells. When, however, the specimens of the large rectosigmoid confluence were obtained for quantitation within a few hours after birth, they were found to exhibit localized expansions with abrupt change to nearly normal calibre, the dilated bowel being thin-walled and containing muscle cells in normal or smaller than normal size and numbers. It is probable that some of those obtained later were at birth similar in their muscle cell dimensions to those examined at birth, but that hypertrophy and hyperplasia had developed secondarily. The muscle cell dimensions of the viscus at birth indicates that the enlargement was not caused by the stimulus of increased work load prior to birth. Those enlargements present at birth are presumably developmental aberrations of expansion or overgrowth of the cloaca when the vesical component is also enlarged, or of its posterior component when the rectum alone is enlarged. When the rectum is abnormally large at birth and is subsequently used in reconstructive surgery of the associated anorectal deformities, it may lead to a large "terminal reservoir" with overflow incontinence which does not respond to aperient or bowel washout treatment. If recognized on the newborn pre and post colostomy radiography, reconstruction should include excision or perhaps trimming, of the dilated segment. The term primary rectal ectasia was recommended as the connotation for this special entity as distinct from megarectum developing to secondary obstruction.