Pediatric Gastroesophageal Reflux Surgery 

  • Author: Tom Jaksic, MD, PhD; Chief Editor: Marleta Reynolds, MD   more...
 
Updated: Apr 19, 2010
 

Background

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

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History of the Procedure

As in many other fields, surgical therapy for gastroesophageal reflux (GER) has evolved a great deal. A few historical procedures of note include the Allison crural repair, the Boerema anterior gastropexy, and the Angelchik prosthesis. Both the Allison and the Boerema repairs have high failure rates and are rarely, if ever, used.[2, 3] The Angelchik prosthesis is a silicone ring that is positioned at the gastroesophageal (GE) junction and prevents reflux. The Angelchik prosthesis was rarely used in children and has been largely abandoned because of a high rate of complications.[4]

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 the image below).[5, 6] First reported in 1991, laparoscopic fundoplication is well studied in adult populations. Laparoscopic fundoplication has also quickly gained acceptance for use in children.[7, 8, 9, 10, 11, 12]

Nissen fundoplication. Nissen fundoplication.
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Epidemiology

Frequency

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;[13] the prevalence decreased to 21% by age 7 months. A one-year follow-up study by the same author demonstrated that vomiting spontaneously resolved in nearly all of these cases.[14] An estimated 85% of premature infants have GER; the vast majority of cases resolve without treatment.[15] Children with neurological 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 neurological impairment than in healthy children (69% vs 47%).[16] Another study found that 65% of patients who underwent antireflux surgery were neurologically impaired.[17]

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Pathophysiology

Nearly all infants have some degree of GER, but it is usually transient and does not cause any morbidity. 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 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 lower esophageal sphincter (LES) and otherwise normal esophageal motor function.[18] Transient LES relaxation occurs normally and is a mechanism to vent air from the distended stomach.[19] 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 an evaluation of 25 pediatric patients with GERD, esophageal manometry and 24-hour pH probes were used to correlate esophageal contractions with acid-reflux episodes.[21] The investigators demonstrated that patients with GERD had significantly fewer and less sustained esophageal contractions than patients without reflux. This may be an important distinction because the presence of esophageal dysmotility in a subset of pediatric patients with GERD could be a relative contraindication to 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 the 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 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. 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.[16]

Children with a history of esophageal atresia and/or tracheoesophageal fistula also have a high prevalence of GER, which often lasts into adulthood.[24, 25, 26] This is likely due to a shortened esophagus and/or superior displacement of the GE junction following surgical repair, abnormal esophageal peristalsis, and delayed gastric emptying (DGE).[27]

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.

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Presentation

Many healthy infants have physiologic reflux. Approximately 40% of healthy infants have at least one episode of emesis a day, with more than 5 mL of nonbilious emesis per episode.[28, 29] These minor reflux episodes (spit-ups) usually resolve by the time the patient aged 6 months and do not cause any serious sequelae. In some children, GER is pathologic, leading to irritability, apnea, recurrent pneumonia, respiratory dysfunction, esophagitis, or failure to thrive.

Generally, a thorough history and physical examination elicits signs and symptoms of reflux. In addition, an infant or child may have a history of frequent emesis, aspiration events, asthma, or feeding difficulty. A careful assessment of growth parameters and nutritional status is an important component of the physical examination and preoperative evaluation. Because one of the indications for antireflux surgery is failure to thrive, operative candidates may be malnourished.

The presenting symptoms of GERD in infants and children differ from those seen in adults and vary with age. Anorexia and feeding difficulty correlate with erosive esophagitis on endoscopy and are common presentations in children aged 1-5 years.[30] Infants may present with frequent regurgitation in addition to feeding difficulties.[31]

Feeding difficulties in infants have been further evaluated in a recent study investigating the clinical outcomes of GERD treatment.[32] In a retrospective review of 28 infants with feeding difficulty prior to GERD treatment, a posttreatment evaluation with both endoscopy and a videofluoroscopy demonstrated marked functional improvement in infant swallowing.

GERD has been closely linked to respiratory problems due to recurrent aspiration of gastric contents.[33] A Pediatric Health Information System Database analysis of 12,067 patients found that GERD was the most common discharge diagnosis in patients admitted with an apparent life-threatening event.[34] Reflux should also be ruled out in a child with recurrent pneumonia or chronic nocturnal cough. Considerable controversy remains regarding whether GERD is associated with sudden infant death syndrome (SIDS) in a temporal or causative manner.[35, 36] The relationship of GERD with childhood asthma is more defined, and the prevalence is thought to be 40%-60%.[37, 38] In a prospective evaluation of pediatric patients with GER and asthma, investigators demonstrated a significant reduction in the use of bronchodilators and inhaled steroids after treatment for reflux disease. This effect was not seen in control patients with asthma and no diagnosis of GER.[39]

Some authors dispute the association between GER and lung disease.[40] The use of multichannel intraluminal impedance has permitted further investigation into the role of nonacid reflux in the pathogenesis of GER–related respiratory disease. An examination of 28 children with persistent respiratory symptoms despite antacid therapy demonstrated that symptoms were more frequently associated with nonacid reflux.[41] A follow-up study of 24 children with asthma found a higher correlation between asthma and reflux detected by impedance (which is able to detect both acid and nonacid reflux) when compared with pH probe alone (acid reflux).[42]

Esophageal mucosal damage from gastric acid exposure is common in patients with GERD and can lead to esophagitis or esophageal stricture. Barrett esophagus, a premalignant process characterized by replacement of the normal squamous cells of the lower esophagus with columnar cells typically found in the stomach, has been linked to chronic reflux in older children. It has been surmised that this metaplasia is due to constant acid exposure during times of healing.[43] Barrett esophagus necessitates serial follow-up with endoscopy and biopsy.

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Indications

The primary indication for antireflux surgery in children with gastroesophageal reflux (GER) is failed medical therapy. Other indications include a history of recurrent aspiration events with or without pneumonia, reactive airway disease, apnea or near-miss SIDS, refractory emesis, failure to thrive, esophagitis, esophageal stricture, Barrett esophagus, and associated anatomic anomalies such as a large hiatal hernia.[44]

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Relevant Anatomy

The anatomy of the esophagus, stomach, and esophagogastric junction 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 distal-most 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.[45, 46, 19] 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. The esophagogastric junction 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.

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, called the Belsey artery.

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

The blood supply of the stomach is rich, with overlap among the vessels. The lesser curve is supplied by the left and right gastric arteries, branches of the celiac trunk and proper hepatic artery, respectively. The greater curve 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 (see the image below).

Relationship of the phrenoesophageal ligament to tRelationship of the phrenoesophageal ligament to the diaphragm and esophagus.
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Contraindications

In some children, reflux is caused by gastric or intestinal motility disorders or by gastric outlet obstruction. Antireflux surgery may be contraindicated in these patients, especially without a gastric emptying procedure. Contrast scintigraphy (milk scan) or upper GI barium study may be used to identify these patients. Antireflux surgery may also be contraindicated in children with esophageal dysmotility disorders. In children with weak or uncoordinated peristalsis of the esophagus, fundoplication may slow passage of food from the esophagus even further.

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Contributor Information and Disclosures
Author

Tom Jaksic, MD, PhD  Professor, Department of Surgery, Harvard University Medical School; Surgical Director, Center for Advanced Intestinal Rehabilitation, Senior Associate in Surgery, Vice-Chairman of Pediatric Surgery, Children's Hospital Boston

Tom Jaksic, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society for Parenteral and Enteral Nutrition, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Melissa A Hull, MD  Fellow, Department of Surgery, Children's Hospital of Boston

Melissa A Hull, MD is a member of the following medical societies: American Society for Parenteral and Enteral Nutrition, International Pediatric Transplant Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Shimae C Fitzgibbons, MD  Research Fellow, Department of Pediatric Surgery, Boston Children's Hospital

Disclosure: Nothing to disclose.

Brian Alan Jones, MD  Research Fellow, Department of Surgery, Children's Hospital Boston and Harvard Medical School

Brian Alan Jones, MD is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Kenneth Azarow, MD  Program Director, Pediatric Surgery, Children's Hospital and University of Nebraska Medical Center; Professor, Department of Surgery, Uniformed Services University of the Health Sciences

Kenneth Azarow, MD is a member of the following medical societies: American Pediatric Surgical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Kurt D Newman, MD  Vice Chairman, Department of Pediatric Surgery, Children's National Medical Center; Professor, Departments of Surgery and Pediatrics, George Washington University School of Medicine

Kurt D Newman, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, and Society of Surgical Oncology

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Michael G Caty, MD  Professor of Surgery and Pediatrics, State University of New York at Buffalo; Consulting Staff, Department of Pediatric Surgery, Children's Hospital of Buffalo

Michael G Caty, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Physician Executives, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Association for Academic Surgery, and Association for Surgical Education

Disclosure: Nothing to disclose.

H Biemann Othersen Jr, MD  Professor of Surgery and Pediatrics, Emeritus Head, Division of Pediatric Surgery, Medical University of South Carolina

H Biemann Othersen Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, American Cancer Society, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society for Parenteral and Enteral Nutrition, American Surgical Association, American Thoracic Society, British Association of Paediatric Surgeons, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, South Carolina Medical Association, Southeastern Surgical Congress, Southern Medical Association, Southern Society for Pediatric Research, and Southern Thoracic Surgical Association

Disclosure: Nothing to disclose.

Chief Editor

Marleta Reynolds, MD  Professor of Surgery, Feinberg School of Medicine, Northwestern University; Head, Department of Surgery and Surgeon in Chief, Head, Division of Pediatric Surgery, Children's Memorial Hospital of Chicago

Marleta Reynolds, MD is a member of the following medical societies: American Pediatric Surgical Association

Disclosure: Nothing to disclose.

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Relationship of the phrenoesophageal ligament to the diaphragm and esophagus.
Arterial blood supply and lymphatic drainage of the esophagus.
Nissen fundoplication.
Toupet partial fundoplication.
 
 
 
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