Dear Editor

Our study shows that the impact on feed buffering on gastric pH is not as great as previously reported and that the relationship between gastric acidity and the acidity of reflux is more complex than previously thought. Nevertheless, it is correct to say that gastric pH buffering and inter-subject variability do interfere with the outcomes of oesophageal pH monitoring, that GOR episodes occur most commonly during the early post- prandial period and that these are not reliably detected using standard pH -based criteria.

However, should we automatically assume that acid GOR is not a pathophysiological factor in infant GOR disease and that measuring it does not provide clinically relevant information? We have previously shown [1] that, of transient LOS relaxation triggered GOR episodes, a greater proportion are acidic in infants with GOR disease compared to asymptomatic controls. We also showed that infants with GOR disease had a median reflux index of 15.1%. These data suggest that, despite the impact of feed buffering on gastric pH, the degree of oesophageal acidification is still significant and probably an important pathophysiological factor in infant GOR disease.

Reference

(1) Omari TI, Barnett CP, Benninga MA, Lontis R, Goodchild L, Haslam RR, Dent J, Davidson GP. Mechanisms of gastro-oesophageal reflux in preterm and term infants with reflux disease. Gut. 2002 Oct;51(4):475-9.

Dear Editor

0mari and Davidson [1] present an interesting paper on monitoring oesophageal and gastric pH in infants using a four channel pH probe. Their use of the three gastric electrodes demonstrates that the intra-gastric fluid bolus is not uniform but has a heterogeneous and probably dynamic pH distribution. We had noted short intervals when recorded oesophageal pH fell below the simultaneously recorded gastric pH [2] and this provides a possible explanation.

Their conclusion that their data redresses the issue of buffering of gastric acidity by milk feeds in preterm infants must however be challenged.

The first point is that the infants studied were a highly selected cohort of healthy, relatively mature (post-menstrual age 35-38 weeks), well grown (weight 2330-3100g) infants with a four hour feed interval. Smaller less mature infants, “ill” infants, or infants suspected of having significant GOR are often fed more frequently than four hourly and may be less able to acidify the gastric contents.

The second point is that the pH profiles (figure 2) do show long periods of buffering. Gastric probe 2 which demonstrates the least buffering show gastric pH > 4 for longer than 70 minutes in 75%, longer than 80 minutes in 50% and longer than 105 minutes in 25% of the infants. Conventional oesophageal pH monitoring will not detect gastro-oesophageal reflux during these post prandial intervals during which the majority of reflux occurs (3). If the duration of buffering in infants fed 2 or 3 hourly was similar this would significantly limit the detection of reflux. It would be of great interest to study infants with shorter feed intervals.

This study provides interesting data with respect to gastric buffering but in our opinion again highlights the potential limitations of conventional oesophageal pH monitoring in infants receiving frequent milk feeds due to the prolonged periods of gastric buffering. A “negative” oesophageal pH probe may reflect gastric buffering rather than the absence of reflux.

References

1. Omari T, Davidson GP. Multipoint measurement of gastric pH in healthy preterm infants. Arch Dis Child fetal and neonatal edition 2003; 88:F517- 520

2. Mitchell DJ, McClure BG, Tubman TRJ. Simultaneous monitoring of gastric and oesophageal pH reveals limitations of conventional oesophageal pH monitoring. Arch Dis Child 2001; 84: 273-276

3. Wenzl TG, Schenke S, Peschgens T, Silny J, Heimann J, an Skopnik H. 2001. Association of apnea and nonacid gastroesophageal reflux in infants: Investigations with the intraluminal impedance technique. Pediatr Pulmonol 31:144-9.

Dear Editor

We congratulate Omari and Davidson[1] on producing more interesting work on intragastric pH monitoring in preterm infants but feel that their results do not fully support their conclusion. This could have read "although the mid and distal stomach are quicker to re-acidify (time pH <4 58.7% and 55.7% respectively) than the proximal stomach (time pH<4 42.2%), these figures are still low". Percentages may be even lower in less mature infants or in infants fed more frequently than 4- hourly. Variability remains a significant problem. The authors report that their results are far less variable than in previous studies and then go on to report highly variable results such as intragastric pH<4 for 15.3-97.7% of the time.

Their recommendation of siting the intragastric probe 9cm below the lower oesophageal sphincter is not practical. First their is potential for the probe to curl back on itself and secondly the infants in their study were nursed in the right lateral position throughout the 4 hours, a difficult technique to maintain for longer monitoring periods.

Although this study makes a valuable contribution to our knowledge of pH monitoring it shows that the problems of extended periods of gastric buffering and inter-subject variability remain substantial.

Reference

(1) Omari T, Davidson GP. Multipoint measurement of intragastric pH in healthy preterm infants. Arch Dis child fetal and neonatal Ed 2003; 88: F517-520.