Gastroesophageal reflux (GER) is an abnormal clinical syndrome characterized by incompetence of the
anti-reflux barrier at the bottom of the esophagus. While all of us vomit or experience heartburn from
time to time, GER becomes a concern when it causes other significant problems (eg, respiratory
problems, failure-to-thrive).
The lower esophageal sphincter (LES) is more of a physiologic valve than an anatomic sphincter. LES
competence results from a balance between the closing mechanisms which comprise it and the opening
forces which try to overcome it. This competence is reached between the 5th and 7th weeks of life.
The closing mechanisms of the LES include the esophageal hiatus (diaphragmatic sling), intra-abdominal
segment of esophagus, angle of His, mucosal rosette, high pressure zone of the lower esophagus, and
positive intra-abdominal pressure. The opening forces acting on the LES include intragastric pressure,
gastric contractions, gastric volume (inversely proportional to gastric emptying), lack of coordination
between peristaltic waves & pyloric opening, and tension of the gastric wall. GER occurs when the
opening forces overcome the closing mechanisms of the LES, either by an increase in the former or a
decrease in the latter.
Acid gastric content is regurgitated into the esophagus in normal people. This physiologic GER produces
no symptoms. Pathologic GER produces symptoms. Once the LES fails, what separates physiologic from
pathologic GER is a combination of the stomach acid "dose" and its clearance from the esophagus. The
symptoms or complications of pathologic GER fall into three categories: respiratory (apnea,
cough/choking, atypical asthma, aspiration pneumonitis or recurrent pneumonia), nutritional (vomiting,
failure-to-thrive), and esophageal (esophagitis, esophageal stricture, esophageal shortening, Barrett's
esophagus).
Predisposing conditions for GER include neurologic impairment, delayed gastric emptying, gastrostomy
placement, repaired esophageal atresia +/- tracheoesophageal fistula, and repaired congenital
diaphragmatic hernia.
A patient presenting with vomiting or other symptoms/signs of GER should be evaluated in light of two
important considerations. First, GER should be demonstrated and other causes for the symptoms/signs
associated with it excluded. Second, there should be a clear cause-and- effect relationship between the
GER and the symptoms/signs. The clinical impression of pathologic GER leads to one or more diagnostic
studies:
A barium swallow or upper gastrointestinal (UGI) series can show GER and also rules out other
anatomic reasons for vomiting (eg, hypertrophic pyloric stenosis, duodenal stenosis, malrotation).
However, this study is only a snapshot of the patient for a few minutes and may miss the GER. With a
strong clinical impression of pathologic GER but a negative barium swallow, a second diagnostic study is
necessary to make or exclude the diagnosis. With a strong clinical impression of pathologic GER and a
positive barium swallow, no other diagnostic studies are absolutely necessary.
24-hour esophageal pH monitoring with a sensitivity and specificity in the range of 90% to 95%
is the single best test for determining pathologic GER. The frequency and duration in which the pH falls
below 4 in the distal esophagus are measured. This study is now generally performed in an outpatient
setting so that recordings are made with the patient engaged in his/her usual activities of feeding,
sleeping, etc.
Esophageal scintigraphy ("milk scan") can demonstrate GER and even aspiration if it occurs. This
study is most commonly used to assess gastric emptying, yielding a per cent at one hour and at more
delayed times if needed.
Esophagoscopy is rarely used to diagnose GER but can demonstrate esophageal complications of
GER (eg, esophagitis, stricture, Barrett's esophagus).
Once GER is diagnosed as the cause of the patient's symptoms/signs, medical or nonoperative therapy is
initiated. The physical measures of more upright positioning and thickened, smaller feedings are
employed. Medications can also be used, including agents that enhance LES pressure and
esophageal/gastric motility (eg, cisapride [Propulcid] -- now not freely available outside of study
protocol; metoclopramide [Reglan]; bethanecol [Urecholine]) and agents that decrease gastric acidity,
such as antacids, histamine H2-blockers (eg, ranitidine [Zantac]), and proton pump inhibitors (eg,
lansoprazole [Prevacid]; omeprazole [Prilosec]; esomeprazole [Nexium]). Distinct improvement with
medical therapy should be seen within two weeks and is ultimately successful in 50% to 80% of patients.
Such medical therapy may allow infants with GER to "outgrow" it.
Operative therapy is necessary in some patients with GER. Absolute indications for surgery include
apnea requiring resuscitation ("aborted SIDS," "ALTE" or acute life-threatening event), recurrent or
continuous pneumonitis, esophagitis, and failure of good nonoperative therapy. Relative indications are
atypical asthma, coughing at night, choking episodes, chronic vomiting, and as an adjunct to feeding
gastrostomy placement in neurologically-impaired patients.
The anti-reflux operation most commonly used in the United States is a fundoplication in which the
fundus of the stomach is wrapped to some degree around the distal esophagus. The goals of
fundoplication are to increase the high pressure zone in the lower esophagus, establish an intraabdominal portion of distal esophagus, and accentuate the angle of His. Types of fundoplication range
from a complete (360-degree) wrap Nissen to partial wraps such as a Toupet (posterior 240- to 270degree) or Thal (anterior 180-degree). They are constructed in a "floppy" fashion so as to avoid
antegrade esophageal obstruction. The more complete the wrap, the more solid the anti-reflux
procedure but the less physiologic it is (ie, patients following Nissen fundoplication are often unable to
burp or vomit if they really need to). I generally use Nissen fundoplications in neurologically-impaired
patients who need gastrostomies and Toupet fundoplications in neurologically-intact patients and those
with impaired esophageal motility (eg, repaired esophageal atresia +/- tracheoesophageal fistula). The
operative approach can either be open via an upper midline or left subcostal incision or laparoscopic
with four to five trocars. Although not yet tested in a prospective, randomized manner, the laparoscopic
approach may result in earlier resumption of enteral feeding, shorter length-of-stay, and less
postoperative pain (especially beneficial in patients with impaired pulmonary function).
Surgery relieves pathologic GER in nearly all patients. It relieves symptoms/signs in more than 90% of
patients (ie, failure reflects the fact that GER probably was not the cause of the clinical disorder). Major
postoperative complications occur in 4% of neurologically-intact and 13% of neurologically-impaired
patients. Complications of fundoplication include gas bloat or retching or inability to burp or vomit, too
tight of a fundoplication, adhesive bowel obstruction, and disruption of the fundoplication ("slipped
wrap") leading to recurrent GER and need for reoperation (overall incidence 6%).
Dr. Breaux is a pediatric surgeon and surgical critical care specialist practicing in Grand Junction,
Colorado.