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Gastroesophageal reflux in infants: a primary care perspective.

Gastroesophageal reflux (GER), defined as the passage of gastric contents into the esophagus, is one of the most common gastrointestinal problems in infants and affects about 50% of healthy, full-term newborns (Jadcherla & Shaker, 2001). Postprandial regurgitation is the most common sign of GER in infants and may range from effortless spitting to forceful vomiting (Sondheimer, 2003). It is common for the pediatric nurse to be approached with questions and concerns from families about GER. In most cases, anticipatory guidance and teaching regarding the natural occurrence of GER and the many non-pharmacological approaches to managing GER are enough to allow for normal growth and development of the child and place the family at ease. Nevertheless, the pediatric nurse should also be able to distinguish GER from gas-troesophageal reflux disease (GERD), which is a pathologic process in infants associated with poor weight gain, signs of esophagitis, persistent respiratory problems, dysphagia, and changes in neurodevelopmental patterns.


Three mechanisms have been identified that allow reflux of the gastric contents across the esophagogastric junction and into the esophagus: transient lower esophageal sphincter relaxations (TLESRs), hypotensive or incompetent lower esophageal sphincter (LES), and anatomic disruption of the esophagogastric junction (e.g., hiatal hernia). TLESRs are mediated primarily through vagal pathways and account for virtually all reflux episodes in healthy individuals and the majority of reflux episodes (50-88%) in those with GERD. TLESRs are primarily triggered by gastric distension after a meal (Orlando, 2001). Pharyngeal stimulation, cholecystokinin, and gastric acid secretion may contribute to an increased rate of TLESRs (Sherman, 2001). Reflux with normal LES pressure may occur with increased abdominal pressure, such as after meals, crying, defecating, and coughing. Infants are more predisposed to "spitting up or vomiting" than are adolescents and adults because of the small reservoir of their esophagus (Herbst, 2000).

Clinical Findings Distinguishing Uncomplicated GER from GERD

Uncomplicated GER. Uncomplicated GER implies a functional or physiological process in a healthy infant with no underlying systemic abnormalities (see Table 1). The incidence of regurgitation is similar in breast-fed and formula-fed infants (Jiang, Ewigman, & Danis, 2001; Orenstein & Shalaby, 1996). Healthy infants may have a high prevalence of reflux symptoms, such as daily regurgitation (40%), mild or absent respiratory symptoms, crying more than one hour per day (17%), arching (10%), or daily hiccups (36%) (Orentsein & Shalaby, 1996). GER that is not complicated by excessive crying, irritability, disturbed sleep, feeding impairment, poor weight gain, or respiratory complications can usually be diagnosed clinically without extensive evaluation. For 85% of infants with uncomplicated GER, the condition is self-limited and usually disappears between ages 6 and 12 months (Sondheimer, 2003).

Gastroesophageal reflux disease (GERD). GERD is a pathological process in infants manifested by poor weight gain, esophagitis, occult blood loss, anemia, persistent respiratory symptoms or complications, and changes in neurobehavior. GERD occurs in approximately 1 in 300 infants (Herbst, 2000). An infant with GERD is likely to have more than five episodes of reflux per day, regurgitate more than 28 g per episode, refuse feeding, experience episodes of apnea, have problems gaining weight, and demonstrate increased irritability (Reust & Blake, 2000). Aspiration pneumonia, chronic cough, wheezing, and other respiratory complications are also associated with GERD (Jung, 2001). Arching and torticollis (Sandifer syndrome) are believed to be related to the esophageal discomfort induced by GERD, as the posturing may help clear esophageal acid (Yellon & Goldberg, 2001). Childhood diagnoses associated with increased risk of GERD include esophageal atresia with repair, neurological impairment and delay, hiatal hernia, bronchopulmonary dysplasia (related to prematurity), asthma, and cystic fibrosis (Jung, 2001).

Differential Diagnosis

The differential diagnosis of GERD encompasses a broad spectrum of disorders of gastrointestinal, respiratory, or infectious origin as outlined in Table 2.

Vomiting. Vomiting, a common problem during the first year of life, may be innocent and benign, but it also can cause complications or indicate serious underlying disease. Vomiting is defined as the forceful expulsion of stomach contents through the mouth via a somatic reflex that makes the abdominal and diaphragmatic muscles contract. Unlike regurgitation, vomiting is preceded by nausea and retching. In infants, pallor, sweating, salivation, and tachycardia suggest nausea (Murray & Christie, 2000). The differential diagnosis of vomiting includes Hirschsprung's disease, necrotizing enterocolitis (NEC), pyloric stenosis, intestinal atresia/stenosis, meconium ileus, malrotation and midgut volvulus, intussusception, peptic ulcer disease and inborn errors of metabolism. Bilious vomiting in infants should always elicit immediate evaluation since it generally indicates a serious condition that may require rapid surgical intervention. The health care provider should consider referring to a surgeon or gastroenterologist any child with bilious vomiting, persistent non-bilious vomiting, or vomiting associated with abdominal pain (Murray & Christie, 2000).

Cow's milk protein allergy (CMA). Iacono et al. (1996) studied the association of GER with CMA in infants during the first year of life. Two hundred four infants who had been diagnosed as having GER on the basis of a 24-hour continuous pH monitoring and histological examination of the esophageal mucosa were evaluated. Diagnostic studies used to test for CMA included cutaneous tests, eosinophil smears of the nasal mucosa, fecal matter, peripheral blood, IgG anti- lactoglobulin levels, double-blind food challenge, and intestinal biopsy. Forty-one percent of the 204 infants with GER were diagnosed with CMA. No differences in distribution were seen for sex, age, or type of feeding (breast milk or formula containing cow's milk) in the infants with GER and CMA. The frequency of this association highlights the importance for the health care provider to screen for possible CMA and perhaps suggest a 2-week trial of protein hydrolysate formula such as Nutramigen[R] or Pregestimil[R] (Rudolph et al., 2001). Children with symptoms of colitis (loose stools, rectal bleeding, abdominal distention, vomiting), atopic dermatitis, rhinorrhea, allergies or family history of allergies should warrant greater suspicion of CMA.

Infection. Vomiting, in combination with other symptoms, may be a sign of sepsis, urinary tract infection, meningitis, or otitis media. Acute gastroenteritis often presents with diarrhea, abdominal pain, and non-bilious vomiting. Rotavirus is generally the pathogen in infants. Bacterial microorganisms such as shigella, salmonella, and campylobacter are more often associated with bloody diarrhea and high fevers. The protozoan, Giardia lamblia, associated with contaminated water and fecal-oral spread in day-care centers, can also cause vomiting and watery diarrhea. Bacterial pathogens in the young infant should be treated. Once the infant is 3 months old, it generally is not necessary to treat salmonella unless it is associated with sepsis (Murray & Christie, 2000).

Rumination syndrome. Infant rumination is the repetitive regurgitation of food from the stomach, which the infant then re-chews, re-swallows, or expels from the mouth. Onset is typically between 3 and 6 months of age. Infant rumination is a rare but serious condition that may develop when there is no reciprocal interaction between the infant and caregiver. The infant learns to bring up gastric contents into the mouth as a means of self-stimulation and to satisfy needs not being met by the caregiver. In contrast to babies with GER, the infant does not ruminate when actively engaged and interested in the immediate surroundings or while sleeping (Malcolm, Thumshirn, Camilleri & Williams, 1997; Murray & Christie, 2000).

Asthma. Gastroesophageal reflux is a potential trigger of asthma. Esophageal acid in the distal esophagus and microaspiration of esophageal acid in the upper airway can produce airway hyper-responsiveness and bronchoconstriction. The prevalence and severity of GER is higher among children with asthma than in control populations (Jung, 2001).

Colic. Colic is a symptom complex of recurrent paroxysmal abdominal pain, presumably of intestinal origin, and severe crying that usually presents in infants younger than 3 months of age (Curran & Lewis, 2000). Colic has been ascribed to several causes, such as immaturity of the gastrointestinal system, inability of the central nervous system to handle the stimulus of the environment, allergies and hypersensitivity, parent-infant interaction mismatch, cultural expectations, and normal variations in behavior (Reust & Blake, 2000). Common clinical manifestations of colic are abdominal distention and tenseness, legs drawn up on the abdomen, clenched hands, cold feet, flushed face or circumoral pallor, and temporary relief with the passage of feces or flatulus (Curran & Lewis, 2000).

Sutphen (2001) states there is little evidence to support the relation between acid reflux and colic. A review of pH probe studies found no correlation between irritability and episodes of reflux. Other research suggests that colic is the primary event that produces emesis and positive test results for reflux. Crying infants swallow air, which may increase the frequency of TLESRs and, thus, promote acid reflux episodes (Kahrilas, Shi, Manka, & Joehl, 2000). Overfeeding colicky infants in effort to pacify them may also increase reflux episodes. Parents and caregivers should be encouraged to document and review with the health care provider the infant's crying behavior, including time of day, length of episodes, and how often the infant is well.

Foreign body aspiration (FBA). Physical findings and complications of FBA vary depending on the nature, location, and degree of obstruction. Some common findings are coughing, dyspnea, wheezing, and cyanosis. It may be acute or gradual in onset. After the initial symptoms, there is often a symptom-free interval that may last from hours to weeks prior to continuing signs and symptoms. Peak age for FBA is toddlerhood, however it should not be overlooked as a causal factor for new-onset respiratory symptoms in the infant. Radiographic findings may show hyperinflation, mediastinal shift, and atelectasis (Goodman & Brady, 2000).

Clinical Assessment

According to the GER Guidelines of the North American Society for Pediatric Gastroenterology and Nutrition (Rudolph et al., 2001), a thorough history and physical examination with attention to warning signals is generally sufficient to allow the clinician to establish a diagnosis of GER, recognize complications, and initiate management.

A thorough prenatal and neonatal history should be obtained including complications with pregnancy or birth, prematurity, newborn screening, growth and development, recurrent illness, surgery, and hospitalization. A family history of significant illness, gastrointestinal or metabolic disorders, and allergy should be documented. The psychosocial functioning of the family should also be assessed.

In the infant with suspected GER or GERD, the health care provider should observe the caretaker feeding the infant. This allows the provider to assess feeding technique, swallow function, as well as infant-caregiver interaction or bonding. The infant's height, weight, and head circumference should be documented at each visit. Significant GER occurring in the absence of emesis may manifest as failure to thrive. Chronic acid reflux into the oral, pharyngeal, and nasal cavities may result in erosion of mucous membranes and dental enamel. Improper oral hygiene techniques may also result in tooth decay, so parents should be questioned about care of their infant's teeth.

A symptom diary is a useful component in gathering a thorough history needed for the differential diagnosis of GER. Clinical data to be obtained in a diary or history is outlined in Table 3.

Observation of feeding behaviors. In the first 3 months of life, the infant is establishing regular patterns of feeding, elimination, sleep, and wakefulness. The baby experiencing illness or discomfort may give unclear signals during feeding, or the caregiver may interpret signals inappropriately (Mason, 2000). Weight gain and effective feeding patterns are important indications of health to the caregiver. Unfortunately, the caregiver and infant may fall into patterns where the feeding process is not satisfactory due to frequent burping, limitation of feeds, or overfeeding in response to the infant's signs of distress or to compensate for food lost in vomiting. During clinic visits, the health care provider should observe a feeding, if possible, paying special attention to the clarity of the infant's cues and the caregivers' ability to effectively respond to those cues (Mason, 2000).

Diagnostic Evaluation

As noted above, for 85% of infants with GER, the condition is self-limited and resolves between 6 and 12 months of age as the infant assumes erect posture and begins solid feedings (Sondheimer, 2001). Infants with signs and symptoms of GERD, such as poor weight gain, esophagitis (hematemesis), or respiratory symptoms require a referral to a pediatric gastroenterologist for further diagnostic tests (Sandritter, 2003). Diagnostic tests commonly used to determine the presence of GERD include the upper gastrointestinal (UGI) series, esophageal pH monitoring, esophageal endoscopy and biopsy, and nuclear scintiscan.

UGI series. The barium contrast UGI series is important, particularly in infants, to identify anatomic causes of recurrent regurgitation or vomiting, such as pyloric stenosis, mal-rotation, hiatal hernia, esophageal stricture, gastric outlet obstruction, or other anatomic abnormalities. The presence of reflux and delayed gastric emptying time may also be identified. However, the UGI series is not sufficiently sensitive or specific to provide a definitive diagnosis of GER (Rudolph et al., 2001).

pH probe. The "gold standard" for the diagnosis of GERD is the 24-hour pH probe. The test is performed by transnasally placing a microelectrode into the lower esophagus, which measure and records intraesophageal pH usually every 4 to 8 seconds (Rudolph et al., 2001). Esophageal pH monitoring via a 24-hour probe provides information about the rate of gastric clearance and frequency of reflux. The pH probe quantifies esophageal acid exposure to determine if an association exists between atypical symptoms (chronic cough, stridor, wheezing, apnea, irritability, or opisthotonic posturing) and acid reflux. One episode of acid reflux is defined by a pH of < 4 for at least 15 to 30 seconds (Sandritter, 2003). The reflux index is the percentage of time during the pH probe study that the pH is < 4. The upper limit of normal for the reflux index in the first year of life is 12% and only 6% in children greater than 1 year of age.

Esophageal endoscopy and biopsy. Endoscopy involves both visualization and biopsy of the esophageal epithelium. Endoscopy can identify underlying conditions affecting the mucosa of the esophagus, stomach, or duodenum that may cause vomiting or increased GER. It generally is reserved for infants suspected of having an underlying inflammatory condition, such as esophagitis, or to define the presence or degree of reflux-induced mucosal injury (Murray & Christie, 2000). Upper endoscopy can help diagnose atypical causes of vomiting such as infectious esophagitis and esophageal or antral webs (Rudolph et al., 2001).

Gastroesophageal scintigraphy. Nuclear scintiscan is performed by oral ingestion of radionuclide-containing formula or food. The stomach, esophagus, and lungs are then scanned for evidence of GER and aspiration. The value of the test is limited, however, due to a lack of normative data. Thus, the role of nuclear scintigraphy in the assessment and management of GERD in infants and children is unclear (Rudolph et al., 2001).

Management of Infants with Uncomplicated GER

Conservative management of the thriving infant with uncomplicated GER (the "happy spitter") is indicated if there are no complications. The pediatric nurse should reassure parents and provide anticipatory guidance regarding the natural course of GER in infants. Non- pharmacological interventions are generally all that are required, and an upper GI series is not required unless there are signs of gastrointestinal obstruction (Rudolph et al., 2001). Other diagnostic tests may be indicated if there are signs of poor weight gain, excessive crying or irritability, sleep disturbances, or respiratory problems (Rudolph et al., 2001). Sutphen (2001) suggests a non-aggressive approach for the vigorous, growing but irritable infant with frequent non-projectile regurgitation. This avoids overuse of tests and encourages parents to accept the infant's symptoms as normal variants of feeding patterns in infancy.

General recommendations. Despite lack of randomized, controlled studies of non- pharmacological management of GER, life-style changes are generally recognized as the appropriate initial management of uncomplicated GER. In infants with GERD, life style changes are recommended in addition to medical therapy. Life style changes include the following modifications: (a) feeding schedule; (b) thickening of feedings; (c) positioning, and (d) formula changes.

Feeding schedule modification. In the overfed infant or infants fed large volumes at infrequent intervals, the volume of formula should be reduced (Brown, 2001; Jiang, Ewigman, & Danis, 2001). Increased frequency of feedings with small volumes has not been proven efficacious, is difficult to implement, and may create distress in a hungry infant. A modest reduction in volume may relieve pressure (Borowitz, 2002; Jiang et al., 2001). When babies cry for extended periods, they fill their stomachs with air, grunt, and strain, all of which tend to make reflux worse (Borowitz, 2002). During feedings, infants should be burped after every 1 to 2 ounces.

Thickened feeds. Thickening feeds with rice cereal (one tablespoon per 2 to 4 ounces of formula) is associated with a decrease in the number of vomiting episodes, but does not improve reflux index scores (Rudolph et al., 2001). Jiang, Ewigman, and Danis (2001) report that thickened formula may reduce the frequency of regurgitation and total volume of emesis. It may also reduce time spent crying and increase time spent sleeping.

Rice cereal used as a thickener increases the caloric density of formula and may cause constipation. Thickened formulas also require enlarged nipple holes to feed, potentially resulting in greater ingestion of air or formula, which can favor regurgitation. Because rice cereal- thickened feedings have 150% of the caloric density of un-thickened feedings, only 65% of the volume needs to be fed per meal; thereby decreasing gastric volume (Orenstein, 2001). In an infant who is solely breast-fed, it is not possible to thicken the feeds unless the mother uses a breast-pump and then feeds the infant, which can be tedious and less desirable.

Commercially available pre-thickened formulas, such as Enfamil AR[R] which contains added rice, may be advantageous because they are nutritionally balanced, convenient, well tolerated, and the viscosity is two-to-threefold less than when rice cereal is added to formula. They can be given without an enlarged nipple hole. The viscosity increases in the acidic environment of the stomach (Brown, 2001; Sherman 2001).

Positioning. Holding the infant in a head-elevated position for 20-30 minutes after feeding may reduce GERD (Farivar, 2001). The prone position has also been shown to reduce reflux, aspiration, and crying time and speed gastric emptying (Sherman, 2001). According to Borowitz (2002), after meals, the best position to place a baby with reflux is lying prone with the head of the bed raised about 30 degrees. Parents should be cautioned that placing the infant in a prone position should only be done when the child is awake and can be continuously observed. Prone positioning during sleep is only considered in unusual cases where the risk of death from complications of GER outweighs the potential increased risk of SIDS (Rudolph et al., 2001). The semi-supine position after feeding, such as when placing the baby in an infant car seat, exacerbates GER and should be avoided (Rudolph et al., 2001; Sandritter, 2003).

Formula change. Many parents and families attribute GER to sensitivities or allergies to milk or formula, and approximately one third of infants with symptoms of GER experience a formula change. However, there is a lack of controlled trials evaluating the efficacy of changing formulas in the management of uncomplicated GER, and parents may come to believe that their child has a disease or illness (Jiang et al., 2001).

True allergy to cow's milk or soy-based formulas occurs in less than 2% of infants and is unlikely to present with vomiting as the only symptom. However, in formula-fed infants, it is reasonable to try a protein hydrolysate or elemental formula, such as Alimentum[R], Nutramigen[R], or Pregestimil[R], for a 2-week period if a cow's milk protein intolerance is suspected (Rudolph et al., 2001). In an infant who is breastfed, temporary elimination of cow's milk protein from the mother's diet may be tried. Temporary carbohydrate intolerance may occur with gastroenteritis, malnutrition, or in pre-term infants, but otherwise is rare in infancy (Brown, 2001).

Evaluation and Management of Infants With Suspected GERD

The North American Society for Pediatric Gastroenterology and Nutrition has published practice guidelines for the evaluation of GERD in infants and children (Rudolph et al., 2001). The guidelines offer the following recommendations for the evaluation and management of infants with suspected GERD, depending upon presenting signs or symptoms:

* In the infant with recurrent vomiting and poor weight gain, despite adequate caloric intake and effective swallowing, the following tests are recommended: CBC, electrolytes, bicarbonate, urea nitrogen, creatinine, alanine aminotransferase, ammonia, glucose, urinalysis, urine ketones and reducing substances, a review of newborn screening tests, and an UGI series to evaluate anatomy.

* In the infant with recurrent vomiting and irritability, in which other causes of vomiting have been excluded, two different approaches may be taken: (a) empiric treatment with either a sequential or simultaneous 2-week trial of hypoallergenic formula and acid suppression may be initiated. If there is improvement, pH monitoring to determine adequacy of therapy or upper endoscopy and biopsy to diagnose esophagitis may be performed; (b) alternatively, evaluation can begin with esophageal pH monitoring to determine if episodes of irritability and sleep disturbance are temporally associated with acid reflux.

* In the infant with feeding refusal, empirical therapy without prior diagnostic evaluation is generally not recommended due to the variety of disorders that may contribute to infant feeding difficulties. However, if there are other signs or symptoms suggestive of GERD, then a limited course of therapy can be considered.

* In infants with frequent apnea or apparent life-threatening events (ALTE) in which the role of GER is uncertain, esophageal pH monitoring may be useful to determine if there is a temporal association of acid reflux with ALTE.

* In infants and toddlers with chronic vomiting or regurgitation and recurrent episodes of cough and wheezing, a 3-month trial of acid suppression therapy of GER is recommended in addition to life style changes (Rudolph et al., 2001).

* pH monitoring is also recommended in certain patients without symptoms of GER. Selected patients include: those with radiographic evidence of recurrent pneumonia, nocturnal asthma more than once per week, patients requiring continuous oral corticosteroids or high dose inhaled corticosteroids, more than two bursts per year of oral corticosteroids, or those with persistent asthma unable to wean from medical management. A trial of prolonged medical therapy for GER is recommended if esophageal pH monitoring reveals increased frequency or duration of esophageal acid exposure (Rudolph et al., 2001).

Pharmacological Management

Persistent problems and complications of GER, despite non-pharmacologic interventions, may warrant pharmacological intervention (see Table 4). If an UGI series has ruled out anatomic causes of recurrent regurgitation, pharmacologic management with the use of an acid suppressant is generally the first line of therapy (Murray & Christie, 2000).

Acid suppressants diminish gastric fluid volume and protect the esophagus from acidic refluxate. This group of medications includes histamine-2 receptor antagonists (H-2 blockers), proton pump inhibitors (PPI), and antacids. H-2 blockers competitively bind to histamine H-2 receptors on parietal cells in gastric glands, thereby inhibiting acid secretion elicited by histamine, but have no effect on acid secretion by acetylcholine or gastrin. Ranitidine (Zantac[R]), an H-2 receptor antagonist, is approved for use in infants and children (Sondheimer, 2003). Follow-up appointments at 4 to 8 week intervals are necessary to assess efficacy of the medication.

Similarly, PPIs decrease the secretion of gastric acid and are antagonists of the proton pump that stimulates the production of gastric acid. Use of a proton pump inhibitor is indicated for infants with recurrent vomiting and failure to thrive, and/or irritability who have not responded to histamine H-2 receptor antagonists. The use of antacids in pediatric GERD is generally not recommended. Significant aluminum absorption from antacids can occur in infants approaching levels reported to cause osteopenia and neurotoxicity (Farivar, 2001). Parents should also be cautioned not to use over the counter preparations of antacids for infants and children. Similarly, prokinetic agents such as metoclopramide (Reglan[R]) may improve gastric emptying and esophageal motor tone, but there are no studies supporting their use in managing symptoms of GERD in infants and children (Sondheimer, 2003).

By 1 year of age most infants with mild to moderate reflux are symptom free and are able to discontinue pharmacological therapy (Mason, 2000). Children over 18 months of age with large hiatal hernias and children who are neurologically impaired respond less well to pharmacological treatment (Sondheimer, 2003).

Surgical Intervention

Surgery may be indicated if reflux causes persistent vomiting with failure to thrive, chronic esophagitis, esophageal strictures, or chronic pulmonary disease that does not respond to 2 to 3 months of pharmacological therapy (Sondheimer, 2003). Surgical management involves the Nissen fundoplication procedure, in which the upper stomach (fundus) is wrapped around the bottom of the esophagus, creating a collar, to augment sphincter pressure (Sherman, 2001; Borowitz, 2002). The surgical success rate based on symptomatic relief in infants and children ranges from 57% to 97% (Farivar, 2001). The mortality rate due to surgery may range from 0 to 4.5%, and complications may occur in up to 45% of cases. The most common complications are breakdown of the fundoplication, small bowel obstruction, infection, atelectasis, perforation, persistent esophageal strictures, and esophageal obstruction (Farivar, 2001).

Family Education

It is important that pediatric nurses be knowledgeable about GER and able to inform the family of the natural course of GER during infancy. Regurgitation is a common and normal occurrence because the lower esophageal sphincter is immature at birth, the esophagus is short, and the stomach is small (Sherman, 2001). Regurgitation at least once a day is reported in half of infants up to 3 months of age, and 67% of 4-month-old infants have a history of regurgitation. Between 6 and 7 months of age, the extent of regurgitation decreases as the infant learns to sit up and solid foods are introduced to the diet. By 10 to 12 months of age only 5% of infants have one episode of reflux a day, indicating that most children "outgrow" GER by 1 year of age (Nelson, Chen, Syniar, & Christoffel, 1997).

The health care provider should educate parents regarding feeding and positioning interventions and reassure parents of their child's health. Growth charts should be shared with parents at each visit to document the infant's continued growth within standard percentiles. Helping the caregiver to understand symptoms and potential complications will enable the caregiver to seek appropriate treatment. When children are treated with medication, the family must know the name and action of the medication, the prescribed dose, potential side effects, and how and when to administer. They will also need to be counseled regarding testing procedures and the evaluation process.

In conclusion, pediatric GER is usually a self-limiting condition, but has the potential of developing into a chronic condition for children. Primary health care providers play an important clinical role in distinguishing uncomplicated GER from pathologic GERD that requires intervention, referral, care coordination, and ongoing family support.
Table 1. Clinical Features Differentiating GER and
GERD in Infants

GER                   GERD

Regurgitation         Regurgitation with weight loss or
with normal           inadequate weight gain
weight gain

No signs or           Persistent irritability, pain in
symptoms of           infants; dysphagia, food refusal;
esophagitis           hematemesis, melena, iron deficiency

No significant        Apnea and cyanosis, sleep disturbance;
respiratory           wheezing or stridor; aspiration
symptoms              or recurrent pneumonia;
                      Chronic cough; hoarseness

No neurobehavioral    Abnormal posturing; (Sandifer's
symptoms              syndrome)

Adapted from: Jung, A. (2001). Gastroesophageal reflux in
infants and children. American Family Physician, 64(11),

Table 2. Differential Diagnosis of GERD in Infants

Gastrointestinal                 Infection

Hirchpsrung's disease            Urinary tract infection
Necrotizing enterocolitis        Otitis media
Pyloric stenosis                 Gastroenteritis
Intestinal atresia / stenosis    Hepatitis
Meconium Ileus                   Meningitis
Malrotation, midgut volvus       Sepsis
Peptic ulcer disease

Respiratory                      Other

Asthma                           Rumination syndrome
Foreign body aspiration          Metabolic disorder
Apnea                            Cow's milk protein allergy
                                 Dysfunctional parent-child

Table 3. History and Assessment of Infants with GER/GERD

Feeding        Breast milk or type of formula fed (number of kcal.oz,
               Fe or low Fe, number of oz taken, preparation errors)
               Cereal and Solids: type, quantity, when introduced
               Frequency of feeds
               Length of time spent feeding: Is the infant hungry/
               eating too fast?
               Position during feeding
               Burping: style, frequency, and effectiveness
               Emesis: "spitting up/wet burps" or forceful/projec-
               tile, number of episodes, quantity, color, presence of
               blood, specify timing with feeds: during, after,

Environment    Quiet and calm, or excessive stimuli/stress
               Caretaker-infant interaction/bonding (focused, eye
               contact, talking)
               Exposure to tobacco smoke

Behavior       Torso hyperextension
               Head tilting
               Choking, gagging
               Food refusal/disinterest or early satiety
               Falling asleep during feeds
               Abdominal cramping/drawing legs upon chest
               Fussiness/irritability, length of time spent crying,
               ability to be consoled

Respiratory    Cough
               Stridor, hoarseness
               Choking, gagging, cyanosis, apnea, struggling to
               Aspiration pneumonia (recurrent or chronic)
               Cyanotic episodes, apnea or apparent life-threatening
               Sleep disturbance/frequent waking

Positioning    After meals: seated, supine, prone, held vertical?
               Activity/vigorous play after feeding?
               Sleeping: supine

Elimination    Stools: frequency, color, consistency, presence of
               mucus or blood, foul smelling
               Urine: Number of wet diapers/day, presence of blood

Table 4. Medication Use in Treatment of GERD in Infants

Type of Medication                 Recommended Oral Dose

Histamine H-2 antagonists
Ranitidine (Zantac[R])             Premature and term infants < 2
Syrup 15 mg/ml                       weeks: 2 mg/kg/day PO divided
                                   Infants > 1 month: 4 - 10 mg/kg/
                                     day PO divided BID
                                   Maximum dose for GERD: 300 mg/QD
                                   Maximum dose for erosive esopha-
                                     gitis: 600 mg/QD
                                   Administer with food
                                   Time to peak serum concentration:
                                     1-3 hours

                                   Infants: 1 mg/kg/day PO divided BID
Famotidine (Pepcid[R])             Maximum dose 80 mg/QD
Liquid 40 mg/5 ml                  May administer with food
                                   Shake suspension vigorously before
                                   Maximum effect: 1-4 hours

Proton pump inhibitors
Lansoprazole (Prevacid[R])         <10 kg: 7.5 mg once daily
Enteric coated capsules: 15 mg,    </= 10-30 kg: 15 mg once daily
30 mg; Granule packets: 15 mg,     >30 kg: 30 mg once daily (may inc-
30 mg                                rease up to 30 mg BID if symptoms
                                     persist after 2 weeks of treat-
                                   Reflux esophagitis: 30-60 mg once
                                     daily for up to 8 weeks
                                   Best if taken 30 minutes before
                                   Capsules may be opened and sprin-
                                     kled in slightly acidic juice
                                     (e.g., apple, orange),
                                     applesauce, or yogurt. Contents
                                     should not be chewed or crushed.
                                   Packets of granules should be mixed
                                     only with water.
                                   Time to peak serum level: 1-2 hours

Omeprazole (Prilosec[R])
Oral susp: 2 mg/ml; Capsules:      1-3 mg/kg/day in two divided doses.
10 mg, 20 mg, 40 mg                Give before meals
                                   Shake vigorously before giving.
                                     Store in refrigerator
                                   Capsules can be opened and mixed
                                     with acid juice such as apple
                                     juice, cranberry juice, or
                                   Maximum action: 2 hours

Type of Medication                 Adverse Reactions

Histamine H-2 antagonists
Ranitidine (Zantac[R])             Fatigue, irritability, constipa-
Syrup 15 mg/ml                     tion, diarrhea, thrombocytopenia,
                                   bradycardia, tachycardia, sedation,
                                   headache, rash, elevated serum
                                   creatinine. Use with caution in
                                   infants with renal or liver impair-

                                   Headache, dizziness, constipation,
Famotidine (Pepcid[R])             diarrhea, nausea, vomiting, brady-
Liquid 40 mg/5 ml                  cardia, tachycardia, thrombocyto-
                                   penia, rash, elevated liver
                                   enzymes, BUN, and serum creatinine.
                                   Use with caution in infants with
                                   renal or liver impairment.

Proton pump inhibitors
Lansoprazole (Prevacid[R])         Diarrhea, abdominal pain, nausea,
Enteric coated capsules: 15 mg,    headache, hyper/hypotension,
30 mg; Granule packets: 15 mg,     fatigue, dizziness, headache, rash,
30 mg                              elevated serum transaminases,

Omeprazole (Prilosec[R])
Oral susp: 2 mg/ml; Capsules:      Diarrhea, nausea, vomiting, abdo-
10 mg, 20 mg, 40 mg                minal pain, constipation, brady-
                                   cardia, tachycardia, headaches,
                                   dizziness, rash, agranulocytosis,
                                   elevated liver enzymes, proteinuria

From: Taketomo, C.K., Hodding, J.H., & Kraus, D.M. (2002). Pediatric
dosage handbook, 9th edition. Hudson, OH: Lexi-Comp, Inc. and the
American Pharmaceutical Association.


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Amy Lynn Arguin, MSN, PNP, is Pediatric Nurse Practitioner, South Hadley, MA and an alumna of Yale University School of Nursing.

Martha K. Swartz, PhDc APRN, BC, is associate Professor and Director, PNP Specialty, Yale University School of Nursing, New Haven, CT.

The Primary Care Approaches section focuses on physical and developmental assessment and other topics specific to children and their families. If you are interested in author guidelines and/or assistance, contact Patricia L. Jackson Allen at
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Title Annotation:Primary Care Approaches
Author:Arguin, Amy Lynn; Swartz, Martha K.
Publication:Pediatric Nursing
Date:Jan 1, 2004
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