Pediatric Gastroesophageal Reflux Surgery

Updated: May 04, 2022
  • Author: Tom Jaksic, MD, PhD; Chief Editor: Robert K Minkes, MD, PhD, MS  more...
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Practice Essentials

Persistent gastroesophageal reflux (GER) disease (GERD) is one of the most frequent disorders for which infants and children undergo abdominal surgery. [1, 2]  However, most children with GERD may be treated nonsurgically. Appropriate therapy for GERD is based on the underlying pathophysiology, the clinical presentation, and accurately interpreted diagnostic test results. [3]

Surgical therapy for GER, like that for many other conditions, has evolved a great deal. Historical procedures of note include the Allison crural repair, the Boerema anterior gastropexy, and the Angelchik prosthesis. Both Allison and Boerema repairs have high failure rates and are rarely, if ever, used. [4, 5]  The Angelchik prosthesis is a silicone ring that is positioned at the esophagogastric junction (EGJ; also referred to as the gastroesophageal junction [GEJ]) and prevents reflux. It was rarely used in children and has been largely abandoned because of a high rate of complications. [6]

Today, both transthoracic and transabdominal fundoplications are performed, including partial (anterior or posterior) and circumferential wraps. The most commonly performed operation today in both children and adults is the Nissen fundoplication, which is a 360° transabdominal fundoplication (see Treatment). [7, 8]  First reported in 1991, laparoscopic fundoplication is well studied in adult populations. Laparoscopic fundoplication has also gained acceptance for use in children. [9, 10, 11, 12, 13, 14, 15]

For patient education resources, see the Children's Health Center, as well as Spitting Up in Infants.



The anatomy of the esophagus, stomach, and EGJ is critical in the understanding of the pathogenesis of reflux.

The proximal esophagus contains the upper esophageal sphincter (UES), which comprises the cricopharyngeus and thyropharyngeus muscles. The body of the esophagus is made up of inner circular and outer longitudinal muscular layers. The proximal third of the esophagus is smooth muscle, which transitions to striated muscle in the distal two thirds. The lower esophageal sphincter (LES) is the distalmost segment of the esophagus (3-5 cm in adults), and its ability to prevent reflux depends on a number of anatomic factors.

As the esophagus passes through the diaphragmatic hiatus, it becomes the abdominal esophagus. The right crus of the diaphragm forms a sling around the esophagus so that the esophagus narrows when the diaphragm contracts. [16, 17, 18] At this level, the phrenoesophageal ligament, which is the reflection of the subdiaphragmatic fascia onto the transversalis fascia of the anterior abdominal wall, also encircles the esophagus (see the image below). The EGJ is in the abdomen and forms the angle of His. The acute angle and the length of abdominal esophagus both contribute to the normal closure of the esophagus when intragastric and intra-abdominal pressures are high.

Relationship of the phrenoesophageal ligament to t Relationship of the phrenoesophageal ligament to the diaphragm and esophagus.

The blood supply of the esophagus is segmental (see the image below). The inferior thyroid artery supplies the cervical esophagus. Branches of the bronchial arteries and branches directly off of the aorta supply the proximal and distal thoracic esophagus, respectively. Finally, branches of the left gastric and inferior phrenic artery supply the abdominal esophagus. A relatively constant branch connects the left gastric and inferior phrenic arteries (the Belsey artery).

Arterial blood supply and lymphatic drainage of th Arterial blood supply and lymphatic drainage of the esophagus.

The blood supply of the stomach is rich, with overlap among the vessels. The lesser curvature is supplied by the left and right gastric arteries, which are branches of the celiac trunk and the proper hepatic artery, respectively. The greater curvature is supplied by the right gastroepiploic artery arising from the gastroduodenal artery and the left gastroepiploic artery and the short gastric arteries originating from the splenic artery. This excellent collateral blood supply of the stomach allows the surgeon to ligate much of the arterial supply (ie, the short gastric arteries during fundoplication) without risk of ischemia.



Nearly all infants have some degree of GER, but it is usually transient and does not cause any morbidity. [2] However, in some children, the reflux is pathologic and persistent, causing feeding difficulties, failure to thrive, aspiration or respiratory complications, esophagitis, and esophageal stricture. GERD occurs on a continuum that ranges from mild physiologic reflux to a severe debilitating problem.

In healthy term and preterm infants, the mechanism of GER is primarily frequent transient relaxation of the LES and otherwise normal esophageal motor function. [19] Transient LES relaxation occurs normally and is a mechanism to vent air from the distended stomach. [18] However, in some children, LES relaxation is frequent and prolonged, leading to pathologic reflux.

Unlike physiologic LES relaxation, GER is primarily observed during episodes of sphincter relaxation unassociated with swallowing. [20] Some children, such as those with neurologic disorders, may be predisposed to frequent LES relaxation, which leads to irritation of the esophageal mucosa by hydrochloric acid. Esophagitis causes further dysfunction of the LES, creating a cycle of continuing injury.

In addition to LES relaxation, esophageal dysmotility may also play a role in pediatric GER. In a study of 25 pediatric patients with GERD, esophageal manometry and 24-hour pH probes were used to correlate esophageal contractions with acid-reflux episodes [21] ; patients with GERD had significantly fewer and less sustained esophageal contractions than those without reflux. This difference may be important, in that the presence of esophageal dysmotility in a subset of pediatric GERD patients could be a relative contraindication for operative management.

The passage of food from the esophagus to the stomach is facilitated by a transient relaxation of the distal esophagus, which is initiated by swallowing-induced peristaltic waves. The resting tone of the distal esophagus is important in preventing reflux of gastric contents into the thoracic portion of the esophagus. The anatomic area integral to the prevention of reflux is the abdominal esophagus, where the high-pressure zone (HPZ) is located.

The HPZ depends on many factors, including an adequate length of intra-abdominal esophagus, an intact phrenoesophageal ligament, a normal diaphragm, and sufficient gastric emptying. Symptoms of reflux tend to occur when the sphincter pressure is in the range of 0-5 mm Hg. [22] About 81% of patients in whom the intra-abdominal esophagus is 1 cm or shorter have reflux, whereas 38% of those with an intra-abdominal segment longer than 3 cm have reflux. [23]

Neurologically impaired children, including those with mental-motor retardation, seizure disorders, and hydrocephalus, appear to have a higher prevalence of GER after age 1 year than neurologically normal children do. Several reasons are postulated for this phenomenon, including a reduction in LES pressure with elevations in intracranial pressure and abnormal esophageal peristalsis secondary to CNS dysfunction. [24]

Children with a history of esophageal atresiatracheoesophageal fistula, or both also have a high prevalence of GER, which often lasts into adulthood. [25, 26, 27] This is likely due to a shortened esophagus or superior displacement of the EGJ following surgical repair, abnormal esophageal peristalsis, and delayed gastric emptying (DGE). [28]

Other factors implicated in the genesis of GER include abnormal or altered anatomy, such as hiatal hernia, short esophagus, and gastrostomy. Medications that decrease LES pressure, such as methylxanthines and calcium-channel blockers, may also exacerbate GER.



The prevalence of GER varies by age. In a study of parent reporting and symptom scores, 67% of healthy infants aged 4 months had GER [29] ; the prevalence decreased to 21% by age 7 months. A 1-year follow-up study by the same author demonstrated that vomiting spontaneously resolved in nearly all of these cases. [30] An estimated 85% of premature infants have GER; the vast majority of cases resolve without treatment. [31]

Children with neurologic disorders also have an increased prevalence of GER. In one referral center, the rate of GER was higher in patients older than 1 year with neurologic impairment than in healthy children (69% vs 47%). [24] Another study found that 65% of patients who underwent antireflux surgery were neurologically impaired. [32]



Long-term data in children have been relatively sparse as compared with data in adults; however, the success rate of antireflux surgery is generally thought to be good. A series of more than 1000 laparoscopic Nissen fundoplications over 10 years in infants and children revealed good outcomes, with a 4% wrap-failure rate. [13] A second report of studies of 1280 children concluded that the median success rate was 86%.

A few reports of objective postoperative testing questioned the benefit of surgery. [33] One study found a beneficial effect of surgery on the rate of reflux-related hospitalizations in children aged 1-4 years, but this effect was not noted in older children. In fact, this study demonstrated that older children with developmental delay experienced an increased rate of reflux-related hospitalizations after surgery. [34]

The 24-hour pH study has been used to objectively evaluate outcomes following antireflux surgery. A prospective review of 53 pediatric patients treated with the laparoscopic Thal fundoplication found that 25% had pathologic reflux at follow-up, though 90% of patients reported that they were symptom-free. This underscores the need for additional objective outcome studies.

Both surgical and medical management tend to have a high failure rate in children with neurologic impairment. [24] Many of these children have serious coexisting morbidity and relatively short life expectancy.

A study of 46 infants examined 5 years after Nissen fundoplication found that 24% had died of other medical problems. [35] Of the survivors, 74% had no recurrent symptoms, 12% required repeat operation or fundoplication, and 45% had had at least one postoperative complication. Another report of 109 children who underwent either Nissen or Boix-Ochoa antireflux procedures, with up to 10-year follow-up, found recurrent reflux in 20% of patients (91% of these cases occurred in the Boix-Ochoa group). [36]

In a study of 300 fundoplications (277 primary, 23 redo) in 279 pediatric GERD patients, Koivusalo et al found that primary fundoplication led to control of symptoms in nearly 90% of patients and reduced the rate of esophagitis as well. [37] Primary fundoplication failed in 15% of patients; factors increasing the risk of failure included an underlying disorder, esophageal atresia, and hiatoplasty. Of the 23 redo procedures, 32% failed.

In a study of 820 pediatric patients who underwent Nissen fundoplication, Banerjee et al found that 190 (23%) underwent further procedures for management of GER at a median age of 21 months (range, 6-186), and of these 190, 90 (47%) had gastrojejunal feeding. [38]  Patients who had previous gastrojejunal feeding were more likely to have a failed redo fundoplication than those who did not have gastrojejunal feeding.