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The offices of pediatric gastroenterologists are filled with infants whose pediatricians have diagnosed gastroesophageal reflux disease. Infants with arching, crying, spitting, and food refusal are being diagnosed with GERD. Although [...]

Background: Abdominal pain in childhood is common yet frustrating when unexplained. Objective: To describe the clinical features and outcome of 8 children (6 girls and 2 boys; mean [[+ or -] SD] age, 13 [+ or -] 2 years) with unexplained abdominal pain who underwent exploratory laparoscopy. Setting: All 8 patients were examined at an academic pediatric gastroenterology center and referred for exploratory laparoscopy because of unexplained abdominal pain. Laparoscopy was offered after family agreement to pursue behavioral management if the pain and disability did not improve. Results: In all 8 children, laparoscopy detected an anomaly at a site corresponding to that of the abdominal pain. Findings were adhesions in 7 children (3 colonic, 2 ileocecal, 1 gastric, and 1 appendiceal) and ovarian torsion in 1 child. At a mean follow-up of 12.6 months, the abdominal pain had completely resolved in 6 children, notably improved in 1 child, and continued unchanged in 1 child. Disability completely resolved in 2 of 3 children. Conclusions: in children with unexplained abdominal pain that is acute in onset, well described, and suggestive of peritoneal involvement, exploratory laparoscopy (1) successfully ends the cycle of abdominal pain in most cases; and (2) commonly identifies abnormalities, usually adhesions. However, whether laparoscopy, the placebo effect, or both promote the healing process is unclear. Further study is needed to develop criteria for referral for laparoscopic evaluation of unexplained abdominal pain. Arch Pediatr Adolesc Med. 1997;151:993-998, Exploratory laparoscopic surgery, of itself, seemed to resolve children's unexplained abdominal pain. A laparoscope is an optical tube system inserted through a small incision in the abdomen wall. In eight cases of children with abdominal pain for which there was no explanation, exploration with a laparoscope was done. In each case, some abnormality was found at the location of the pain, but no further procedure was done. In seven of the eight cases, the pain either disappeared or improved considerably. It is not clear what caused the improvement in the patients' conditions.

An approach is presented for treating infants who develop 'short gut colitis', or inflammation of the small intestine in babies who have already developed short bowel syndrome. This is a condition in which digestion and absorption of nutrients is impaired because a significant amount of intestine has been lost due to disease or abnormal development. Total parenteral nutrition (TPN; the delivery of nutrients intravenously), a relatively recent therapeutic approach, has dramatically improved the outcome for most infants with short bowel syndrome. Some, however, develop short gut colitis. Sixteen infants (aged 2 to 20 months) with an average small intestine length of approximately 24 centimeters were studied. They had bloody diarrhea, which was not obviously the result of infection, as well as signs of poor carbohydrate absorption. All patients were fed both parenterally (via a thin tube inserted into a major vein) and enterally (by mouth) with formula. Their symptoms had begun when enteral feeding was being introduced. Examinations of the bowel (by sigmoidoscope) and biopsies were performed in several cases; the histopathological results (of tissue examination under a microscope) are presented. The infants' symptoms improved when enteral nutrition was given at less than full strength or stopped, implying that the colitis may have been a result of malabsorption of nutrients in the formulas. Suggestions are presented concerning the management of these patients and the medications that seemed most beneficial. Sulfasalazine appeared to be most effective in decreasing bowel inflammation. Short gut colitis is best treated soon after symptoms appear, and early treatment ultimately makes it easier to wean infants from TPN. (Consumer Summary produced by Reliance Medical Information, Inc.)

Resolving chronic constipation in children EXPRESS STOP Chronic constipation in children: Boys develop chronic retentive constipation with soiling more often than girls. The child is unaware of and unable to [...]

Gastroesophageal reflux (GER) is common in infants and children, accounting for 20% of all outpatient visits to a typical pediatric gastroenterologist. The author describes the clinical presentations of functional, primary, and secondary pathologic GER in childhood and evaluates diagnostic tests appropriate to each.

Gastroesophageal reflux is common among young infants and may cause significant morbidity in a minority of affected patients. Recent clinical research has changed early assumptions about pathogenesis, and refinement in diagnostic techniques have improved the ability to identify and treat these patients.

This retrospective study was conducted to determine the incidence of cholestasis and liver failure in patients with intestinal resection in the neonatal period who subsequently become dependent on parenteral nutrition support and to assess the significance of associated clinical factors-gestational age, birth weight and length; length of bowel resected; presence of ileocecal valve; enteral feeding history; and infection to the incidence and severity of cholestasis.

Twenty-four infants, 3–35 months of age, with histories of apnea or chronic lung disease underwent nighttime polysomnography and esophageal pH monitoring. Fifteen infants had pathological levels of gastroesophageal reflux on esophageal pH monitoring, and 9 had normal study results (symptomatic controls). Partition of sleep stages, sleep efficiency, and frequency of arousals to electroencephalographic stage 0 were the same in both groups. During sleeping reflux episodes, defined as reflux starting during sleep stages 1–5 or reflux episodes consisting of >50% of sleep stages 1–5, there was a 50% decrease in the amount of stage 0 electroencephalogram pattern compared with nonreflux sleep, and a compensatory increase in the non-rapid eye movement sleep stages. Reflux onsets in patients with pathological reflux were evenly divided between stages 0, ½, and 5. Onset of reflux occurred rarely during sleep stages 3 and 4. Slight body movement accompanied the onset of 62.5% of sleep reflux episodes in symptomatic controls and 64.7% in patients with pathological gastroesophageal reflux. Arousals to stage 0 electroencephalogram occurred with equal frequency in sleep reflux episodes of symptomatic controls and patients, and frequency did not increase over the observed value for nonreflux time. There were no differences between the sleep patterns of infants with and without pathological gastroesophageal reflux; nor were there decreases in arousals from sleep in infants with pathological reflux. However, reflux occurring during sleep in all infants studied was characterized by a significant decrease in stage 0 (waking) electroencephalogram.

Thirty infants < 12 mo old (19 with pathologic gastroesophageal reflux and 11 symptomatic controls) underwent continuous monitoring of distal esophageal pH with simultaneous pharyngeal and multiple-site esophageal manometry to compare acid clearance times of awake and asleep reflux episodes. While awake, acid clearance times of the two groups were equivalent. While asleep, mean acid clearance time increased in subjects with pathologic reflux > 500% while remaining essentially unchanged in symptomatic controls. No difference in minimum pH attained during sleep reflux, in percentage of swallows resulting in esophageal peristalsis, or in the frequency of secondary peristaltic waves was found to explain the difference in sleeping acid clearance times in the two groups. However, there was a significant difference between the groups with respect to swallowing rate (p < 0.01). During sleeping reflux episodes, subjects with pathologic reflux swallowed 0.5 ± 0.1 times per minute (mean ± SEM), whereas controls who refluxed swallowed 3.5 ± 1.3 times per minute. During awake reflux episodes the swallowing rates were equivalent in the two groups, 4.1 ± 0.4 and 4.7 ± 0.7 per minute, respectively. We conclude that low swallowing rate during sleeping reflux episodes is primary to the delayed clearance of sleeping reflux in these infants.

We have characterized the gastroesophageal reflux (GER) episodes which occurred during sleep in 28 infants with pathologic gastroesophageal reflux and 10 symptomatic age-matched controls without gastroesophageal reflux. We describe three kinds of episodes during the sleeping period-awake episodes which occur completely during electroencephalogram (EEG)-defined wakefulness associated with clinical evidence of the waking state (62 episodes), episodes occurring during EEG-defined sleep which have a rapid drop in pH at their onset (119 episodes), and episodes occurring during EEG-defined sleep in which the esophageal pH drifts down slowly over a period up to 30 min (113 episodes). Only 9 of the 10 control subjects experienced any reflux episodes during monitoring. The total number of episodes of reflux in controls (34) was less than the total number in reflux subjects (260). Controls did, however, experience all three types of reflux episode. Awake episodes all had a rapid drop in pH at their onset and were characterized by a short acid clearance time (2.0 ± 0.3 min in reflux patients and 1.0 ± 0.2 min in controls). The sleep episodes with rapid onset had longer mean acid clearance time than the awake episodes, significantly so in GER subjects (20.1 ± 6.8 min in reflux subjects and 2.6 +1.3 min in controls). Body movement was noted at the onset of 93.4% of rapid-onset sleep episodes in reflux subjects and 88.9% in controls. Body movement was also common at the termination of rapid-onset sleep episodes (77.8% of rapid-onset episodes in reflux subjects and 80.0% in controls). The drift-onset sleep episodes in GER subjects were characterized by a low frequency of body movements at their onset (body movement seen in 34.9% of drift-onset episodes), a higher minimum pH (3.6 ±0.1 versus 2.8 ± 0.2 drift-onset vs. rapid-onset episodes), a tendency to start in the deeper EEG sleep stages when compared to rapid-onset sleep episodes, and a decreased frequency of movement arousal. Mean acid clearance time of drift-onset sleep episodes was similar to rapid-onset sleep episodes in GER subjects (15.3 ± 6.1 min). Similar characteristics were noted in the few episodes of drift-onset reflux observed in the control subjects except that drift episodes had significantly greater mean acid clearance time than rapid-onset episodes (19.4 ± 9.9 min). We conclude that sleep reflux episodes with drifting onset are a significant part of total reflux occurring during the sleeping period. The similarities between rapid- and drift-onset sleep episodes with respect to acid clearance time, and presence of movement at the termination suggests that the mechanisms of clearance of these two episodes may be similar. The differences in onset characteristics between these two episode types, however, suggests the possibility that they may be initiated by different mechanisms

We made continuous, simultaneous recordings of esophageal pH from three sites in the esophageal body, for 18–24 h, in 11 children with normal prolonged distal esophageal pH studies (Group I) and in 14 children with abnormal distal esophageal pH recordings (Group II). A flexible catheter housing four antimony microelectrodes was used, and data were stored in a portable recorder. A computer allowed for evaluation of the percent of time esophageal pH was <4.0, number of reflux episodes per hour, acid clearance time, and the duration of longest reflux episode. Recordings made while subjects were upright or recumbent could be distinguished and analyzed separately. In the recumbent position, comparison of pH recordings from distal, middle, and proximal esophageal pH electrodes in Group I showed significant decreases in the percent of time spent with pH <4.0, reflux episodes per hour, acid clearance time, and duration of longest reflux episode in the proximal esophageal sites, with a near negligible total acid exposure in the most proximal electrode. In Group II subjects, however, comparison of recumbent recordings from distal, middle, and proximal esophagus indicates that the proximal esophagus is highly exposed to acid reflux and that the decrease in acid exposure from distal to proximal esophagus in reflux patients is not proportionally as great as that of Group I. The data suggest that in the recumbent position, the ability of the subjects with abnormal reflux scores to protect the upper esophagus is less than that of subjects with normal amounts of distal esophageal acid exposure.

Summary: Since the original description of solitary rectal ulcer by Cruveilheir in 1830, about 250 cases have been reported (1). The condition most frequently presents in adults between 30 and 50 years of age. There are very few pediatric case reports and none have come from North America. We report here a 13-year-old boy with solitary rectal ulcer syndrome and a review of the pediatric experience with this rare condition.

Gastric pH was recorded with an intragastric pH electrode for 12 h in two groups of healthy, preterm infants with similar birth weights (range 1.4 to 2.0 kg). Group I infants (n = 13) were less than 7 days old and Group II infants (n = 10) were 7–15 days old. Infants were fed three formula feedings and one clear liquid feeding during the study. In Group I, mean gastric pH measured at 15-min intervals was above 4.0 for 3 h after either feeding. In Group II mean gastric pH was lower particularly after clear liquid feedings, where it remained below pH 4.0 for the entire 3-h postprandial period. The percent of monitored time at gastric pH less than 4.0 was low in Group 1–15.2 ± 4.2% and 20.6 ± 6.4% after formula and clear liquid, respectively. The percent time was greater in Group II-42.7 ± 8.0% and 61.9 ± 7.3% after formula and clear liquid, respectively. In the younger preterm infant, gastric pH does not appear sufficiently low to support peptic activity.

Lower esophageal sphincter (LES) pressure, as well as esophageal peristaltic amplitude, duration, and velocity were measured in 16 infants with gastroesophageal reflux before administration of subcutaneous bethanechol, and at 10, 20, and 30 min after. Seven infants received 0.1 mg/kg, and 9 received 0.2 mg/kg. Significant increases in LES pressure occurred at both doses and lasted for 20 min. The amplitude and duration of peristaltic contractions were increased only after the larger bethanechol dose, and the increases were of greater magnitude in the distal esophagus than in the middle esophagus. The velocity of peristalsis decreased significantly in both the lower and middle esophagus, but only after the larger dose of bethanechol. Bethanechol had no effect on any motor function of the upper third of the esophagus. The changes in esophageal peristalsis produced by bethanechol may improve the efficiency of distal esophageal acid clearance and thus may be responsible in part for the therapeutic effect of bethanechol in infants with gastroesophageal reflux.

We studied a 5 year old girl from early infancy with severe chronic diarrhea, steatorrhea and growth failure. Intestinal structure, pancreatic function, liver function and structure and a laparotomy all were normal. During the first 2 years of life BA levels in duodenal juice were consistently below the critical micellar concentration. In recent studies fecal BA were 7 times normal, serum BA by radioimmunassay failed to rise significantly after meals or after oral taurocholate and in duodenal juice, dihydroxy predominated over trihydroxy BA. Pool sizes of cholate and chenodeoxycholate, by isotope dilution were reduced to 6 and 23%, serum cholate T½ was 12% and chenodeoxycholate 7% of normal. Vitamin B12 absorption (Schilling test) at age 4 years was normal. These data lead us to conclude that our patient, who now thrives, suffers from a specific congenital defect of ileal transport of bile acids causing a depleted BA pool and steatorrhea. This defect has not been reported previously.

It is generally believed that recurrent vomiting occurs with increased frequency among institutionalized retarded children. To test this hypothesis and to determine the causes of vomiting, we evaluated 136 pediatric residents of a school for the retarded. Recurrent vomiting (emesis > eight times per month) was present in 20 residents (14.7%). Fifteen of the vomiters were evaluated by radiographic techniques, esophageal mannometry, upper intestinal endoscopy and esophageal acid reflux test (ART). GER was demonstrated by x-ray and/or ART in 11 of these 15 subjects (73%). Of those with GER 10/11 had occult blood in stool or emesis in the preceding year; 3/11 were anemic (Hg < 11.5g%). Six had hiatal hernia. Five were said to be inducing emesis. Seven of 11 had resting lower esophageal sphincter pressure (LESP) < 15mmHg, abnormal esophageal peristalsis and endoscopically demonstrated esophagitis. In the 4 patients with LESP > 15mmHg, no esophagitis or abnormal peristalsis was present. The 11 patients with GER did not differ from the non-vomiting residents with respect to age (14.5 vs 13.9 yrs), incidence of seizures, spasticity or ability to walk. GER patients had significantly lower mental age (6.4 vs 16.6 mos) and higher incidence of kyphoscoliosis (54 vs 23%). Onset of vomiting was after age 2 years in 9 of the 11 patients.GER associated with a high incidence of hiatus hernia and esophagitis is common among retarded children who vomit. Vomiting appears later in life than in normal children with GER. Anatomic abnormalities accompanying kyphoscoliosis may contribute to the development of GER.