Journal of Pediatric Gastroenterology & Nutrition:
Commentary on “Esophageal Endoscopic Dilations”
Dall’Oglio, Luigi; De Angelis, Paola
Digestive Surgery and Endoscopic Unit, Bambino Gesù Children Hospital, Rome, Italy.
Address correspondence and reprint requests to Luigi Dall’Oglio, MD, Digestive Surgery and Endoscopic Unit, Bambino Gesù Children Hospital, 00165 Rome, Italy (e-mail: firstname.lastname@example.org).
Received 22 November, 2011
Accepted 13 January, 2012
The authors report no conflicts of interest.
See “Esophageal Endoscopic Dilations” by Lakhdar-Idrissi et al on page 744.
The article of Lakhdar-Idrissi et al (1) is interesting because it deals with an important topic that is often underestimated as a routine clinical problem. Esophageal stricture is a common pediatric disorder and dilation is a common pediatric procedure, sometimes difficult to perform and with possible serious complications. To avoid esophageal perforation and for a good outcome, esophageal strictures need a correct diagnosis, evaluation, and treatment. Regarding the stricture etiology, the authors report a series of peptic strictures that are not common in pediatric literature, which shows a particular environmental situation in Morocco. Even if the Riad Centre is a referral center, the high incidence of peptic strictures is a sign that gastroesophageal reflux disease (GERD) needs correct diagnosis and careful treatment to avoid this severe complication. Perhaps the patients come from rural areas with difficult access to health care resulting in delay in GERD diagnosis and proper treatment. In fact, in these patients, the diagnosis of GERD was made based on the appearance of dysphagia that represents the complication's sign, such as stricture and consequent malnutrition. In the period 1995–2005, we observed 28 children (20 boys, mean age 8.4 years, range 2–13) with peptic stricture; we planned surgery only after stricture resolution with proton pump inhibitors and dilations. Nissen fundoplication was performed with associated pyloromyotomy in case of delayed gastric emptying. The authors do not describe Barrett esophagus; this problem was frequently noted in the follow-up of our series (19/28, 67.8%). We observed the Barrett esophagus after a mean of 6 years (range 1–12) even if the fundoplication seemed continent in 18 of 19 and with normal pH-metry. The 1 patient with Nissen failure underwent a new Nissen with good outcome but with persistent Barrett esophagus. These children are still in endoscopic follow-up. The stricture etiology could also involve other diseases, such as eosinophilic esophagitis. The authors (1) do not describe the performance of routine histopathology to exclude this pathology as a possible cause of esophageal stricture. This unusual incidence of esophageal stricture could be caused by eosinophilic esophagitis that may be related to specific environmental situations or eating habits. Many authors suggest routine multiple biopsy along the entire length of the esophagus in cases of noncaustic or postsurgical strictures. (2,3).
A second diagnostic aspect, well described in the article, is the important role of esophageal follow-through, not only for stricture diagnosis but above all for a correct therapeutic strategy. To avoid complications, it is important to know the stricture extension and whether it is located along the esophagus's multiple stenosis. The presence of a tortuous stricture or the presence of a pseudodiverticulum could represent a possible obstacle to the safe guidewire (GW) passage, with a high risk of a wrong track. Concerning the endoscopic treatment, the authors do not report the use of radiological control to verify the correct positioning of the GW through the stricture into the stomach. It is sometimes possible to avoid radiological control by palpating the abdomen and feeling the GW in the stomach (we use a stiff type, the 0.035 mm Boston Scientific Amplatz Super Stiff [Natick, MA]). With long and sometimes tortuous strictures, as in caustic forms, many authors suggest radiological control to ensure correct GW passage along the esophagus and to avoid the wrong track. (4,5). Endoscopic check alone, as reported by the authors (1), could fail, with a possible risk of perforation; however, the authors reported a perforation incidence of 2 in 247 procedures (2.8%), which is not higher than seen in the literature (0.47%–3.8%) (6). The incidence of perforation has been related to the type of dilator, either the semirigid Savary-Gilliard bougies or hydrostatic balloon dilators. The perforation rate has been estimated to be 5% to 8% (6) or 6% (4) for balloon dilations and 0.18% (5) or 5.6% (7) for bougienage. The Savary-Gillard bougies are more reliable than balloon dilators in consolidated and fibrotic strictures such as congenital stenosis and old caustic stenosis (8,9). Different experiences and results were reported with semirigid or balloon dilators (5–9) and these differences often depend on the availability of different instruments. It must be emphasized that single-use balloon dilators are more expensive (€100–250 each) than the reusable semirigid Savary-Gillard dilators. We agree with the use of hydrostatic dilators in epidermolysis bullosum strictures, as reported elsewhere (10). To avoid esophageal perforations, either with balloons or with semirigid bougies, proper training in the procedures and prudence remain of basic importance, as is “not increasing the diameter of the balloon catheter by >1 catheter size (2–3 mm in diameter) for each dilatation in patients requiring serial dilatations”(6). In cases of suspected perforation, a prompt and correct endoscopic and radiological diagnosis of the entity and the site of the lesion is the cornerstone of successful conservative treatment.
1. Lakhdar-Idrissi M, Khabbache K, Hida M. Esophageal endoscopic dilations. J Pediatr Gastroenterol Nutr 2012;54:744–7.
2. Furuta GT, Liacouras CA, Collins MH, et al. Eosinophilic esophagitis in children and adults: a systemic review and consensus recommendations for diagnosis and treatment. sponsored by the American Gastroenterological Association (AGA) Institute and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. Gastroenterology 2007; 133:1342–1363.
3. Shahzad G, Mustacchia P, Frieri M. Role of mucosal inflammation in eosinophilic esophagitis: review of the literature. ISRN Gastroenterol 2011;2011:468073.
4. Alshammari J, Quesnel S, Pierrot S, et al. Endoscopic balloon dilatation of esophageal strictures in children. Int J Pediatr Otorhinolaryngol 2011; 75:1376–1398.
5. Piotet E, Escher A, Monnier P. Esophageal and pharyngeal strictures: report on 1862 endoscopic dilatations using the Savary-Gilliard technique. Eur Arch Otorhinolaryngol 2008; 265:357–364.
6. Lan LCL, Wong KKY, Lin SCL, et al. Endoscopic balloon dilatation of esophageal strictures in infants and children: 17 years’ experience and a literature review. J Pediatr Surg 2003; 38:1712–1715.
7. Jayakrishnan VK, Wilkinson AG. Treatment of oesophageal strictures in children: a comparison of fluoroscopically guided balloon dilatation with surgical bougienage. Pediatr Radiol 2001; 31:98–101.
8. Romeo E, Foschia F, de Angelis P, et al. Endoscopic management of congenital esophageal stenosis. J Pediatr Surg 2011;46:838–41.
9. Foschia F, De Angelis P, Torroni F, et al. Custom dynamic stent for esophageal strictures in children. J Pediatr Surg 2011; 46:848–853.
10. de Angelis P, Caldaro T, Torroni F, et al. Esophageal stenosis in epidermolysis bullosum: a challenge for the endoscopist. J Pediatr Surg 2001;46:842–7.
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