Managing gastro-oesophageal reflux disease in children

Gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease (GORD) have a higher prevalence among infants than among children or adults. This is linked to the immaturity of the oesophagus and stomach and the higher liquid intake of infants. Genetic factors could also be contributory in some families. Clinical symptoms in infants are mainly regurgitation and vomiting, which usually disappear between 1 and 3 years of age. Symptoms in children are similar to those in adults. Treatment in children depends on age and GORD severity. With GOR or mild GORD, particularly in infants, explanation and reassurance together with thickening of formula feed and lifestyle changes are usually effective. Prokinetics either have unproven efficacy (metoclopramide, domperidone) or have been withdrawn (cisapride). Chronic antacid therapy is not recommended. In moderate to severe GORD, histamine-2-receptor antagonists and particularly proton pump inhibitors (PPIs) are effective, especially when oesophagitis is present. PPIs, in particular omeprazole and lansoprazole, have proven efficacy in infants and children. They are well tolerated, with pharmacokinetics similar to those in adults. However, dosages should be adapted in neonates and children under 10 years old. Fundoplication should be avoided before 2 to 3 years of age if possible.     

Complications of gastro-oesophageal reflux disease

Gastro-oesophageal reflux disease (GORD) is on the rise with more than 20% of the western population reporting symptoms and is the most common gastrointestinal disorder in the United States. This increase in GORD is not exactly clear but has been attributed to the increasing prevalence of obesity, changing diet, and perhaps the decreasing prevalence of H. pylori infection. Complications of GORD could be either benign or malignant. Benign complications include erosive oesophagitis, bleeding and peptic strictures. Premalignant and malignant lesions include Barrett's metaplasia, and oesophageal cancer. Management of both the benign and malignant complications can be challenging. With the use of proton-pump inhibitors, peptic strictures (i.e., strictures related to reflux) have significantly declined. Several aspects of Barrett's management remain controversial including the stage in the disease process which needs to be intervened, type of the intervention and surveillance of these lesions to prevent development of high grade dysplasia and oesophageal adenocarcinoma.     

Smoking and gastro-oesophageal reflux disease

The role of smoking in the pathogenesis of gastrooesophageal reflux disease has been controversial since the early 1970s when Stanciu reported the two to be 92% epidemiologically associated (a study subsequently challenged by inconsistencies in the observational data). Mechanistically, reflux disease is caused by excessive oesophageal acid exposure, which is potentially attributable to excessive reflux events and/or prolonged acid clearance. Currently, the best available pH monitoring data confirm that smoking increases oesophageal acid exposure. Smoking reduces lower oesophageal sphincter (LOS) pressure and predisposes to strain-induced reflux. Consistent with this, smoking has been shown to cause an increased number of reflux events that are not attributable to increased transient LOS relaxations, but rather are associated with deep inspiration and coughing. Once reflux occurs, acid is cleared from the oesophagus by a two-step process consisting of oesophageal peristalsis followed by neutralization of the residual acid by swallowed saliva. Smoking prolongs acid clearance by decreasing salivation. The effects of smoking on LOS tone and acid clearance are most likely mainly due to nicotine but are incompletely understood. Transdermal nicotine has similar effects to smoking on LOS pressure and salivation. Thus, although perhaps not a dominant risk factor, smoking and nicotine impact on pathophysiological variables of gastro-oesophageal reflux disease. In itself, smoking cessation is unlikely to cure severe gastrooesophageal reflux disease, but, along with appropriate pharmacological therapy, it may be beneficial.     

Pathophysiology of gastro-oesophageal reflux disease

Gastro-oesophageal reflux disease (GERD), defined as symptoms or mucosal damage caused by reflux of gastric contents into the esophageal body, is a multifactorial disorder. Malfunctioning of the anti-reflux barrier at the esophagogastric junction, consisting of the right diaphragmatic crus and the lower esophageal sphincter (LES), is the pivotal abnormality. Other factors such as impaired esophageal clearance, decreased resistance of the esophageal mucosa and delayed gastric emptying, may contribute.     

The extent of duodenogastric reflux in gastro-oesophageal reflux disease

BACKGROUND: It is known that duodenogastro-oesophageal reflux (DGOR) increases with worsening gastro-oesophageal reflux disease (GORD). It is unclear whether this is accompanied by increasing duodenogastric reflux (DGR). OBJECTIVE: To investigate the extent of DGR in a control group and 66 patients with GORD, using the technique of ambulatory gastric bilirubin monitoring. METHODS: Sixty-six patients with reflux symptoms (30 grade 0 or 1 oesophagitis (group 1), 16 grade 2 or 3 oesophagitis (group 2), 20 Barrett's oesophagus (group 3)) and 17 healthy controls were studied. All underwent oesophageal manometry followed by 24-h ambulatory oesophageal and gastric pH monitoring and gastric bilirubin monitoring. RESULTS: Median per cent total oesophageal acid exposure (pH < 4) was significantly less in the control group (0.6%) than in group 1 (2.8%, P< 0.05) and groups 2 and 3 (7.5% and 7.8% respectively, P< 0.001). There was no significant difference between any group in median per cent total time gastric pH was greater than 4. There was no significant difference in median per cent total gastric bilirubin exposure (absorbance > 0.14) between any group. However, in each group gastric bilirubin exposure was greater in the supine position than the upright position, being significantly greater in the control group (P< 0.05) and group 1 (P < 0.001). CONCLUSIONS: Gastric bilirubin exposure is similar across the spectrum of GORD severity. It is greater in the supine than in the upright position.     

Gastric emptying and duodeno-gastro-oesophageal reflux in gastro-oesophageal reflux disease

BACKGROUND: Previous studies present conflicting results regarding relationship between gastric emptying and gastro-oesophageal reflux disease. Reflux of duodenal content to oesophagus is generally considered to be associated with more severe disease. AIM: To assess presence of a gastric emptying disorder in persons with reflux of duodenal contents to oesophagus and to identify any correlation with gastric emptying and oesophageal motility. METHODOLOGY: A total of 15 subjects with (B+) and 15 subjects without (B-) bile reflux to oesophagus determined by 24-hour bilirubin monitoring were studied with scintigraphic solid gastric emptying and 24-hour oesophageal manometry. RESULTS: There was no difference in lag phase [median 23.7 (range 10.8-44.0) vs 24.6 (8.1-40.1) min], half emptying time [74.6 (48.0-93.6) vs 82.8 (54.4-153.9) min] or emptying rate [0.89 (0.59-1.34) vs 0.83 (0.36-1. 15)%/min] for B- and B+ subjects, respectively. In addition, there was no difference in emptying rate of gastric fundus between B- and B+ subjects. Subjects with bile reflux had less effective oesophageal contractions of oesophageal body [9.4(3.3-37)%] compared to subjects without bile reflux [32(19-47)%, p = 0.002]. However, there was no correlation between oesophageal motility and gastric emptying. CONCLUSION: Results suggest that a gastric emptying disorder is a less likely contributing cause of bile reflux to the oesophagus, but bile reflux is associated with less effective oesophageal motility.     

Proximal gastric tone in gastro-oesophageal reflux disease

BACKGROUND/OBJECTIVE: Abnormal gastric function may be involved in the pathogenesis of several gastrointestinal functional disorders. This study evaluated gastric tone in gastro-oesophageal reflux disease (GORD). METHODS: Proximal gastric tone was measured with an electronic barostat in fasting conditions and after oral ingestion of a 200 ml/200 kcal liquid meal in 10 patients with GORD, with control groups consisting of 10 patients with dysmotility-like dyspepsia and 16 healthy subjects. RESULTS: Minimal distending pressure was increased in GORD patients compared to dyspeptic patients (P < 0.04) and controls (P< 0.001). Maximal postprandial gastric relaxation was significantly increased in GORD patients (430 +/- 95 ml) compared to dyspeptic patients (200 +/- 152 ml, P < 0.0001) and controls (342 +/- 88 ml, P= 0.05). Endoscopy-negative and mild oesophagitis patients had more profound maximal relaxation than patients with moderate or severe oesophagitis, whereas those with dyspepsia had significantly reduced gastric relaxation compared to GORD patients and controls (P < 0.002). CONCLUSIONS: In GORD, the postprandial gastric relaxation is more pronounced than in normal and dyspeptic patients. The pathophysiological relevance of this abnormal motility pattern remains to be determined.     

Secondary oesophageal peristalsis in gastro-oesophageal reflux disease

BACKGROUND AND AIMS: To evaluate the status of secondary oesophageal peristalsis in gastro-oesophageal reflux disease (GORD) and the effect of healing of oesophagitis on these abnormalities. METHODS: Twenty-one patients diagnosed with GORD and 10 control subjects in the same age group were studied. Primary peristalsis was elicited by 10 5 mL water boluses and secondary peristalsis by 10 20 mL boluses of air injected 15 cm above the lower oesophageal sphincter. RESULTS: The pattern of primary peristalsis was normal in a significantly lower number of patients compared with control subjects, six patients (28.6%) versus seven controls (70%), (P<0.05). Similarly, the number of subjects with a normal pattern of secondary peristalsis was also lower in the patient group (zero vs three; P<0.05). A normal primary peristaltic response occurred with 71 (33.8%) of the 210 water boluses in the patients and 73 (73%) of the 100 water boluses in the control subjects, respectively (P<0.001). A normal secondary peristaltic response was seen with 15 (7.1%) of 210 air boluses in patients and 32 (32%) of 100 air boluses in the control subjects (P<0.001). The amplitude of secondary peristaltic waves and the duration of contraction (mean+/-SEM) were significantly lower in patients compared with the control subjects (43.5+/-4.7 vs 89.0+/-13.1 and 3.4+/-0.8 vs 3.9+/-0.3, respectively; P=<0.05). In the 13 patients in whom repeat evaluation was performed after healing of oesophagitis, there was no significant change in the number of patients with normal peristaltic response, number of normal responses to air and water boluses, or amplitude, duration and velocity of peristalsis. CONCLUSION: Significant abnormalities of secondary oesophageal peristalsis occur in patients with GORD and these are not reversed by healing of oesophagitis.     

Ethnic differences in gastro-oesophageal reflux disease.

OBJECTIVES: To see whether the anecdotal statement that gastro-oesophageal reflux disease is less common in blacks than in white Caucasians is true. DESIGN: Study of the racial origin of adult patients who, at endoscopy, have oesophageal damage due to gastro-oesophageal reflux. SETTING: Gastroenterology unit of a teaching hospital in inner city Birmingham, UK. MAIN OUTCOME MEASURE: Ethnicity and endoscopic grade of oesophageal damage (reflux oesophagitis) were recorded in every patient in whom oesophageal damage due to gastro-oesophageal reflux was diagnosed. RESULTS: Over the eight-year period 1989-1996, 1101 patients with endoscopically diagnosed grades I-V reflux oesophagitis have been seen, of whom 893 (81.9%) were white, 156 (14%) were Indian and 52 (5%) were Afro-Caribbeans. There were fewer patients with reflux oesophagitis from the two non-white ethnic groups than would be expected from their prevalence in the catchment population, and severe reflux oesophagitis was less common than expected in the two non-white groups. In all groups, patients with grades III, IV and V reflux oesophagitis were older than patients with grades I and II disease. Whites tended to be older than Afro-Caribbeans or Indians. CONCLUSION: There were fewer non-whites with reflux oesophagitis than would be expected but the reasons for this are unclear. This study has been useful as a pilot but further studies are needed in ethnically mixed non-migrant populations both in hospital, primary care and the community to clarify racial differences in reflux oesophagitis.