Effect of the dietary fiber glucomannan on chronic constipation in neurologically impaired children.

OBJECTIVE: Inadequate dietary fiber intake is a widely accepted explanation for chronic constipation in children with severe brain damage. The aim of our study was to evaluate the efficacy of glucomannan, a soluble fiber, as a treatment for chronic constipation in these children. STUDY DESIGN: Twenty children with severe brain damage and chronic constipation were randomly assigned to double-blind treatment with either glucomannan (n = 10) or placebo (n = 10) for 12 weeks. Stool habits, total and segmental gastrointestinal transit times, and anorectal motility were evaluated in all children before and after the treatment period. RESULTS: Glucomannan significantly increased (P <.01) stool frequency, whereas the effect of placebo was not significant. Laxative or suppository use was significantly reduced (P <.01) by glucomannan but was not affected by placebo. Clinical scores of stool consistency were significantly improved and episodes of painful defecation per week were significantly reduced by glucomannan (P <.01) but not by placebo. However, neither glucomannan nor placebo had a measurable effect on total and segmental transit times. CONCLUSIONS: In neurologically impaired children, glucomannan improves stool frequency but has no effect on colonic motility.

Upper gastrointestinal tract motility in children with progressive muscular dystrophy.

Gastric emptying was evaluated in 15 children (mean age, 8.0 years) with progressive muscular dystrophy to detect early gastrointestinal smooth muscle involvement; 10 of the children also underwent esophageal manometry. Clinical evidence of skeletal muscle dysfunction was minimal in 14 of the 15 patients; 10 of them had no gastrointestinal symptoms. Gastric emptying studies were performed by using 500 muCi of technetium 99m-sulfur colloid bound to a scrambled egg, and scintigraphic measurements were made continuously for 60 to 90 minutes. Gastric emptying studies and manometric tracings were compared with those from 11 children (mean age, 8.4 years) without gastrointestinal or muscular disorders. Mean (+/- SD) percentage retention of gastric isotope was significantly greater in patients with muscular dystrophy than in control subjects. No differences were found between the two groups in distal esophageal motility or in upper and lower esophageal sphincter pressures or relaxation. Contraction amplitudes in the upper portion of the esophagus, however, were significantly lower in patients with myopathy than in control subjects. These data suggest that dysfunction of smooth muscle of the upper gastrointestinal tract is detectable in children with muscular dystrophy early in the course of the disease, even when gastrointestinal symptoms are absent and skeletal muscle symptoms are minimal.

Esophageal motor abnormalities in children with gastroesophageal reflux and peptic esophagitis.

Esophageal motility was studied in 26 children with gastroesophageal reflux. In 11 patients (group A), esophagitis was severe; in the remaining 15 (group B), either mild or no microscopic changes were found. Lower esophageal sphincter pressure and amplitude, as well as velocity and duration of esophageal pressure waves, were manometrically measured. All patients underwent a 12-week intensive antacid course. Manometric tracings, blindly read, were compared with those of 16 age-matched children with emesis without proven reflux (group C). Among the variables analyzed, amplitude of the motor waves was significantly lower in patients with severe esophagitis than in group B and C patients (P less than 0.01). Nonspecific motor defects (simultaneous, broad-based, double-peaked waves) were more commonly present in group A. At the end of therapy, symptoms had either disappeared or significantly improved. Endoscopic and histologic studies showed disappearance of the severe inflammatory changes. Manometry, repeated in patients with cured severe esophagitis, showed normalization of the amplitude and significant decrease of the nonspecific motility abnormalities. We conclude that severe gastroesophageal reflux disease in children causes esophageal motor dysfunction, resulting from esophageal inflammation. The occurrence of esophageal motility disorders only in patients with severe esophagitis and its disappearance after therapy may account for the favorable course of reflux disease in infancy.

Gastrointestinal transit time, frequency of defecation, and anorectal manometry in healthy and constipated children.

Total gastrointestinal transit time (TGITT), frequency of defecation, and anorectal manometry were evaluated in 63 pediatric patients referred for chronic nonorganic constipation; in 39, segmental transit times of the right and left colon and rectum were also measured. TGITT was significantly longer in chronically constipated children than in matched normal controls. Although bowel frequency was highly significantly correlated with TGITT in patients with prolonged transit time, not all children with prolonged TGITT had reduced bowel frequency. Moreover, not all children with constipation had prolonged TGITT. In children with idiopathic chronic constipation, slowing of intestinal transit occurred most frequently at the level of the distal colon and rectum. Anorectal motility variables were not significantly different in children with functional chronic constipation and in normal children. Maximal resting and pressure and mean intrarectal distending volume causing threshold inhibition in constipated patients did not significantly differ from the control values. Therefore, anorectal manometry did not detect relevant motor abnormalities in constipated children.