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Gastroesophageal reflux disease (GERD) in infants and children

Brandi Barnhill, MSN, FNP

University of Cincinnati

Abstract

Gastroesophageal reflux is the passage of gastric contents into the esophagus and is a normal physiological process that occurs throughout the day. Gastroesophageal reflux disease (GERD) is a condition, which develops when the reflux of stomach contents cause troublesome symptoms and/or complications. In children GERD can be especially difficult to diagnose, symptoms may mimic other disease processes or cause other illnesses. This article will present the evidence of GERD and its correlation with other diseases, acute and chronic illnesses in infants.

Key Words: Gastroesophageal reflux disease, infants and children, esophagitis

Introduction

Gastroesophageal Reflux disease (GERD) is a common disease in both children and adults. With GERD there is dilation of the esophagus, which allows acid contents to pass into it. GERD is most likely caused by inappropriate relaxation of the lower esophageal sphincter which fails to prevent gastric acid reflux into the esophagus, prolonged esophageal clearance of the gastric fluxate, and impaired esophageal mucosal barrier function. Intraabdominal pressure, hormones, neurologic control, and age influence the lower esophageal sphincter. Reflux is a normal physiological process in newborns because the neuromuscular control of the gastroesophageal sphincter is not fully developed. This normal physiological process is usually considered harmless because most episodes are brief and do not cause esophageal injury or other complications. Reflux most frequently occurs in premature infants and decreases during the first 6 to 12 months of life. Reflux is considered GERD when the reflux episodes are associated with symptoms or complications. Evidence suggests that there is a relationship between GERD and reactive airway disease, asthma, otitis media, esophagitis, apparent life-threatening events (ALTE), upper respiratory infections (URI), and laryngopharyngeal reflux.

Pathophysiology

According to McCance, Huether, Brashers, and Rote (2010) possible causes of inappropriate sphincter relaxation are delayed maturation of the lower esophageal sphincter and impaired hormonal or neurotransmitter response mechanisms. In children lower esophageal sphincter integrity is maintained by the location of the gastroesophageal junction in a high-pressure zone within the abdomen, mucosal gathering within the sphincter, and the angle at which the esophagus is inserted into the stomach. If any of these factors are altered reflux persists. The irritation to the mucosa from the reflux results in deterioration of the esophageal epithelium and stimulation of the vomiting reflex.

Classifications

In a review by Mushtaque (2010) GERD is classified into two groups on the basis of endoscopy findings. If there is mucosal damage GERD is classified as either erosive esophagitis or Barrett’s esophagus. If no mucosal damage is found GERD is classified as endoscopy-negative reflux disease, symptomatic GERD, or non-erosive reflux disease. The Montreal definition of GERD is the first global consensus definition, which defines GERD as a condition that develops when the reflux of the stomach contents causes troublesome symptoms and/or complications. The Montreal definition classified GERD into esophageal and extraesophageal syndromes. Esophageal syndromes is that which has symptoms and esophageal injury, whereas extraesophageal syndromes have established or proposed association with GERD and acknowledges that while evidence is sufficient to link syndromes to reflux, it is insufficient to establish causation. Thus, esophageal syndrome would be GERD with mucosal damage such as erosive esophagitis and Barrett’s esophagus, and if no mucosal damage is found this would be considered extraesophageal syndrome as in endoscopy-negative reflux disease, symptomatic GERD, or non-erosive reflux disease.

Epidemiology/Prevalence

Gastroesophageal reflux is very common in infants and decreases in frequency toward the age of one year. Many of the episodes of reflux result in regurgitation into the oral cavity. The decreased frequency of reflux and regurgitation or vomiting is such that it is unusual in children older than 18 months old (Winter, 2011). Regurgitation is a valuable clinical index for gastroesophageal reflux.

GERD occurs in 85% of premature infants and 20-40% of infants 6 months of age or less, and persists in 10-20% of children 12 months of age and older. (Ryan-Wenger, 2007). According to Winter (2011) in one study of healthy infants 13 months and younger, regurgitation was reported in approximately half of the 0 to 3 month-old infants with at least one episode per day, and only 5 percent of 10-12 month old infants. In an article by Bharwani (2011) it states physiologic regurgitation can occur in up to 70% of completely healthy newborns and infants, and resolves without intervention in 95% of infants by 12-14 months of age.

Predisposing Conditions/High Risk Groups

There are certain conditions in children which predispose them to an increased incidence, relapse and chronicity of GERD symptoms. Conditions include neurologic impairment, repaired esophageal atresia, hiatal hernia, chronic respiratory diseases like cystic fibrosis (CF) and genetic conditions like Down syndrome and Cornelia de Lange syndrome (Bharwani, 2011). There is also a familial link between Barrett’s esophagus, strictures, and adenocarcinoma with GERD and children who have a family history are at an increased risk.

Signs and Symptoms

Symptoms are caused by exposure of the esophageal epithelium to refluxed gastric contents. Excessive vomiting occurs in 85% of affected infants during the first week of life and others symptoms are usually present by 6 weeks (McCance et.al, 2010). If the vomiting is forceful it must be differentiated from pyloric stenosis. In reflux that persists through childhood chronic cough, wheezing, and recurrent pneumonia are common. Inadequate retention of nutrients, delay in growth and weight gain may be seen with repeated vomiting. Pain, bleeding, and later stricture formation, and abnormal motility are present with esophagitis. According to McCance et. al, 2010 approximately 10-20% of children with GERD also have iron deficiency anemia, which is caused by frank or occult blood loss. Intestinal symptoms of GERD include regurgitation, abdominal pain, heartburn, and dysphagia (Ryan-Wenger, 2007). Other symptoms include chronic cough, sore throat, hoarseness, halitosis, dental erosion, pharyngitis, and otitis media (Ryan-Wenger, 2007). There may also be concerns about feeding difficulty reported by parents. These include pulling from the bottle or breast, refusing to eat, crying, choking, coughing, and wheezing during feeding. Periods of apnea, irritability, continuous unexplained crying, weight loss, recurrent respiratory infections, pneumonia, and bloody emesis are also reported in younger children. Heartburn is also a common complaint among older children and is defined as a burning sensation behind the sternum that may take the quality of pain. This is a symptom of GERD with or without esophagitis. Dystonic head posturing, torticollis, and opisthotonic back movement known as Sandifer Syndrome is an uncommon, but specific manifestation of GERD.

Esophageal Manifestations

Esophageal manifestations include excessive regurgitation, feeding refusal, anorexia, unexplained crying, chocking, gagging, coughing, sleep disturbance, and abdominal pain. Typical reflux syndrome is also an esophageal manifestation and is a term used for older children and adults who report heartburn with or without regurgitation (Bharwani, 2011). Syndromes with esophageal injury including reflux esophagitis, reflux stricture, Barrett’s esophagus, and Adenocarcinoma are also considered esophageal manifestations.

Extraesophageal Manifestations

Extraesophageal manifestations of GERD include asthma, pulmonary fibrosis bronchopulmonary dysplasia, chronic cough, chronic laryngitis, hoarseness, pharyngitis, sinusitis, serous otitis media, pathological apnea, bradycardia, and apparent life threatening events. There is also a definite association between Sandifers syndrome and dental erosion with extraesophageal manifestations. Other extraesophageal symptoms include globus, vocal cord granuloma, subglottic stenosis, laryngeal cancer, bronchitis, bronchiectasis, aspiration pneumonia, idiopathic pulmonary fibrosis, and noncardiac chest pain. Gastroesophageal reflux is seldom the sole cause of extraesophageal disorders but may be a contributory factor.

Complications of GERD

According to Burns, Dunn, Brady, Starr, and Blosser (2009) complications of GERD include chronic cough, FTT, irritability, malnutrition, and esophageal injury secondary to gastroesophageal reflux results in bleeding, stricture formation, and Barrett’s esophagus. GERD is also associated with significant asthma, pneumonia, laryngeal disorders, apnea, and may have a role in the initiation of otitis media with effusion.

Strictures

About 5% of patients with esophagitis have stricture formation (McPhee & Papadakis, 2011). Stricture formation is manifested by the gradual development of solid food dysphagia that progresses over months to years. Because there is also an association between strictures and concomitant columnar metaplasia of the squamous epithelium, endoscopy with biopsy is mandatory in all cases to differentiate between peptic stricture and esophageal carcinoma.

Barrett Esophagus (BE)

The most severe complication of GERD is Barrett’s metaplasia. There is a strong association between BE and esophageal adenocarcinoma. BE is considered to be a precancerous lesion and an accurate diagnosis is imperative. BE is most commonly associated in patients with long-standing reflux symptoms and is characterized microscopically by the replacement of the normal squamous epithelium of the esophagus with specialized columnar epithelium known as intestinal metaplasia (Bharwani, 2011). Endoscopically a tongue-like extension of salmon-colored mucosa from the gastroesophageal junction is seen.

Esophageal adenocarcinoma in children is very rare and most cases are associated with BE. The chief clinical concern in the pediatric population is to prevent children with GERD from developing BE, and to detect those children with GERD who are at risk for developing BE (Jadcherla & Nurko, 2011).

Hemorrhage and Perforation

Patients with esophageal erosions and ulcers may develop chronic bleeding and iron deficiency anemia. Most patients with reflux esophagitis have little or no evidence of gastrointestinal bleed. Perforation of the esophagus is a rare complication. It usually develops as a consequence of an esophageal ulcer that results in mediastinitis (Bharwani, 2011).

Dental Erosion

Dental erosion in GERD is created by an acid-induced loss of dental hard tissue without the involvement of bacteria. The pH of the regurgitated acid is approximately 1-2, which is much lower than the critical pH 5.5 of enamel dissolution (Wang, Zhang, Wang, Jiang, Guo, 2010). The severity of erosion appears to be correlated with proximal upright reflux.

Diagnostics

History and Physical

In the text by Burns, et.al (2009) important information to include in the history includes careful birth, medical, and social history. Any concerns about feeding difficulty, pulling away from the bottle or breast, refusing to eat, crying, choking, coughing, wheezing, apnea, weight loss, irritability, continuous unexplained crying, recurrent respiratory infections, pneumonia, and bloody emesis in young children should also be addressed. Any history of failure to thrive, acute life-threatening events, and sandifer syndrome are also important pieces to include in the history. Other symptoms to address include heartburn, painful belching, headache, dyspnea, abdominal pain, stool pattern changes, dental caries, and recurrent pneumonia. The physical examination may reveal signs of failure to thrive, torticollis, hoarseness, anemia, and tooth erosion resulting from destruction of enamel by gastric acids caused by frequent vomiting. The physical examination may also reveal a rash, recurrent diarrhea, persistent vomiting, or early-morning vomiting.

Symptom-based diagnosis

According to the Montreal definition GERD can be diagnosed in primary care on the basis of symptoms alone without additional diagnostic testing. For this method a well-taken history including symptom frequency, duration, and severity are important for diagnosis however this method cannot be used to diagnose complications of GERD (Mushtaque, 2010).

pH Monitoring

Esophageal pH monitoring measures the frequency and duration of the episodes of acid reflux and is widely used as an index of esophageal acid exposure. According to Bhatia & Parish (2009) an episode of acid reflux is defined as esophageal pH of less than 4 for a minimum of 15 to 30 seconds. The percentage of the total time the pH is less than 4 is called the reflux index and is considered the most valuable and valid measure of reflux. In infants to 1 year old the normal reflux index can be defined as up to 12% and children over 1 the normal is up to 6%. The 24-hour test is considered the most reliable, because asymptomatic episodes can occur. Endoscopic and histopathological esophagitis is strongly associated with abnormal esophageal pH monitoring. Monitoring of esophageal pH is also helpful to assess the adequacy of acid suppression and guide therapy and may be useful to determine risk for upper airway complications of GERD. pH monitoring does not detect nonacid reflux episodes that frequently occur in infants. Multichannel monitoring is recommended for neonates since it will detect nonacidic reflux. The impedance technique is used to detect the nature of the reflux (liquid, gas, or mixed) and also defines the extent of migration of the refluxate and establishes relationships between reflux and symptoms such as coughing.

Radiography

An upper gastroenterology (GI) series is useful to detect anatomic abnormalities such as hiatal hernia, or to detect problems such as stricture or pyloric stenosis (Bhatia & Parish, 2009). The upper GI has sensitivity from 31 to 86% and a specificity of 21 to 83% and positive predictive value of 80 to 82% when compared with pH monitoring (Bhatia & Parish, 2009).

Sonography

In a study by Dehdashti, Dehdashtian, Rahim, & Payvasteh (2011) the abdominal esophagus was measured from its entrance into the diaphragm to the base of the gastric folds in 235 fed neonates and infants. GERD was diagnosed using the sonography and was confirmed by a barium meal. The study found that neonates and infants with reflux had a significantly shorter abdominal esophagus than subjects without reflux. The results of the study suggest sonography can be used as a single and adequate diagnostic test for GERD.

Endoscopy and Biopsy

Endoscopy and biopsy are useful in determining the presence and severity of esophagitis, strictures, and Barrett’s esophagus. Eosinophils and neutrophils may also be detected. However, these procedures have not been routinely utilized in neonates and infants and criteria to define esophagitis and its severity have not been validated in the pediatric population.

Role of Genetics

In a study by Guarino, Cheng, Harnett, Biancani, Altomare, Panzera, Behar, & Cicala (2010) the recent detection of transient receptor potential channel vanilloid subfamily member-1 (TRPV1; also known as vanilloid or VR receptors) is further discussed. According to the study these VR receptors found in the esophageal mucosa of non-erosive reflux disease (NERD) patients may offer an explanation for the visceral hypersensitivity reported in NERD. TRPV1 may be an important role in human perception because in healthy volunteers capsaicin and acid plus capsaicin instillation into the esophageal lumen produces significant chest pain and heartburn and sensitizes the esophagus to different stimuli. The TRPV1 activation not only evokes sensation of burning pain but also induces inflammation by the release of substance P, calcitonin-gene-related peptide, and platelet activating factor. NERD patients with resistance to acid suppressive therapy drugs may be due to a more sensitive esophagus because of enhanced excitability of visceral sensory neurons due to over expression of TRPV1 in the epithelial layer and in afferent fibers of the lamina propira.

A gastroesophageal reflux disease susceptibility gene in pediatric and adult GERD patients known as Collagen type III alpha I (COL3A1) has been shown to be genetically associated with Hiatus Hernia (HH) in adult males (Bharwani, 2011). Recently, the proteinase-activated receptor-2 (PAR-2) expression in the esophageal mucosa of patients with GERD was shown to be 7- to 10-fold unregulated (P4.0 in infants with persisting reflux symptoms. Acta Pædiatrica, 95, 176-181. doi:10.1080/08035250500327609

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