Central Annals of Otolaryngology and Rhinology

Cite this article: Karen Vanessa SS (2018) Dysphagia in Children: Gastroesophageal Causes. Ann Otolaryngol Rhinol 5(2): 1208.

*Corresponding author

Stave Salgado Karen, Pediatric doctor specialist in Child Gastroenterologist. Ex-scholarship of the Gastroenterology Service of Hospitalde Pediatría S.A.M.I.C. Prof. Dr. Juan P. Garrahan, Buenos Aires – Maipú 863, CP 1006, Buenos Aires, Argentina, Tel: +54 1126387622; E-mail:

Submitted: 12 March 2018

Accepted: 05 April 2018

Published: 06 April 2018

ISSN: 2379-948X

Copyright© 2018 Karen Vanessa

OPEN ACCESS

Keywords•Dysphagia•Swallowing disorders•Children•Pediatric dysphagia

Abstract

Dysphagia is any disruption to the swallow sequence that results in compromise to the safety, efficiency, or adequacy of nutritional intake. Pediatric dysphagia has focused largely on a number of specific populations at risk for swallowing difficulties, such as children with cerebral palsy, acquired/traumatic brain injury, other neuromuscular disorders, craniofacial malformations, airway malformations, congenital cardiac disease, and gastrointestinal disease.

The gastroesophageal disorders that cause dysphagia and swallowing/feeding difficulties, such as gastroesophageal gastroesophageal reflux disease, eosinophilic esophagitis and achalasia need an early diagnosis because they can compromise quality of life and produce complications at the patients.

ABBREVIATIONSUES: Upper Esophageal Sphincter; OA: Oesophageal Atresia;

TEF: Tracheo-Oesophageal Fistula; GER: Gastroesophageal Reflux; GERD: Gastroesophageal Reflux Disease; Eoe: Eosinophilic Esophagitis; LES: Lower Esophageal Sphincter; VFSS: Videofluoroscopic Swallow Study; FEES: Fiberoptic Endoscopic Evaluation of Swallow; UGI: Upper Gastrointestinal Series.

INTRODUCTIONDysphagia refers to problems in any of phases of swallowing.

When referring to pediatric populations, the terms feeding and swallowing difficulties are more frequently used and are becoming more common, particularly in infants born prematurely and in children with chronic medical conditions [1,2]. General diagnostic categories associated with pediatric swallowing and feeding difficulties include neurological conditions, anatomical anomalies, gastrointestinal disorders, conditions affecting sucking swallowing and breathing coordination, and genetic conditions [2].

The consequences of dysphagia can be debilitating for children, as it may lead to failure to thrive, respiratory complications, and compromised quality of life therefore early diagnosis is critical [1,2].

The objective of this clinical review is to provide a global understanding of the common gastroesophageal causes of dysphagia in children in order to make a suitable diagnosis and treatment.

Normal swallowing

The act of swallowing includes four stages: preparatory, oral,

pharyngeal an esophageal phase. In the first phase, also known as the oral preparatory phase, the food is taken into the oral cavity, chewed and moistened with saliva, and prepared into a bolus, which is held between the hard palate and oral tongue. This process first becomes evident at approximately 6 months of age [1]. The oral phase consists of salivation, mastication and the transportation of the bolus towards the pharynx. In the pharyngeal phase the bolus is transported through the pharynx to upper esophageal sphincter (UES); and the last phase include transportation of the bolus through the esophagus to the stomach [3].

The sequence of events during the pharyngeal and esophageal phases remains the same throughout a person’s life, and these events can be summarized as follows: (a) closure of the nasopharyngeal port through movement of the velum; (b) pharyngeal closure through contraction of the superior, middle, and inferior pharyngeal constrictors; (c) closure of the vocal folds with brief cessation of respiration; (d) hyolaryngeal excursion and closure of the larynx through epiglottic tilt; (e) opening of the upper esophageal sphincter through relaxation of the cricopharyngeus muscle and biomechanical forces contributed through hyolaryngeal excursion, and (f) peristaltic contraction of the esophagus to move the food or liquid into the stomach [3].

In neonates and young infants, all components of swallowing are reflexive and involuntary. Later in infancy, the oral phase comes under voluntary control, which is important to allow children to begin to masticate solid food.

Abnormal swallowing

Any disruption to the swallow sequence is called dysphagia,

Review Article

Dysphagia in Children: Gastroesophageal CausesStave Salgado Karen Vanessa*Pediatric doctor specialist in Child Gastroenterologist, Ex-scholarship of the Gastroenterology Service of Hospitalde Pediatría, Argentina

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Karen Vanessa (2018)Email: kstave@gmail.com

Ann Otolaryngol Rhinol 5(2): 1208 (2018) 2/5

that results in compromise to the safety, efficiency, or adequacy of nutritional intake [3].

Approximately 1% of children in the general population will experience swallowing disorders, though the incidence rate is much higher in infants born prematurely and in children with chronic medical conditions [4,5].

It is important distinguish dysphagia as a skill-based disorder, which is very different from a behaviorally based feeding disorder. Behavioral feeding disturbances occur when a child is unwilling to consume a fluid/food despite sufficient physical skills to do so.

The common presentations of pediatric dysphagia symptoms are [3]:

• Oral phase: Absent oral reflexes, primitive/neurological oral reflexes, weak suck, uncoordinated suck, immature biting and/or chewing, disordered biting and/or chewing, poor bolus propulsion, poor bolus containment.

• Pharyngeal phase: Laryngeal penetration, aspiration, choking, pharyngeal residue, nasopharyngeal reflux.

Causes of dysphagia

The causes of dysphagia in pediatric populations are often somewhat different than in adult patients, and children can present with multiple variations of swallowing impairments affecting any or all of the phases of swallowing. Table 1 summarizes common causes of dysphagia in pediatric patients [3,6,7].

Gastroesophageal causes of dysphagia

Oesophageal atresia: Oesophageal atresia (OA) is a congenital malformation, characterized by an interruption in the continuity of the oesophagus and have an incidence of around 1:2500 live-births. It may be divided anatomically into 5 types with the most common being oesophageal atresia with a distal tracheo-oesophageal fistula (TEF) found in around 85% cases. The condition consists of a discontinuity or atresia of the oesophagus; with the majority of infants exhibiting a connection or fistula between the oesophagus and trachea. The exceptions to this are children born with an isolated OA and those with an H-type TEF [8,9].

Dysphagia is a common problem in children with repaired OA, with ranges between 45-70%. The etiology of dysphagia may include inflammatory or anatomic causes such as peptic esophagitis, eosinophilic esophagitis, anastomotic stricture, congenital stenosis, peptic stricture, post-fundoplication obstruction, vascular anomalies, anastomotic diverticulum, mucosal bridge, and inlet patch. In the absence of the latter causes, esophageal dysmotility remains the accepted explanation [9,10].

Dysphagia can present with simply a complaint of difficulty in swallowing (50%), nausea (27%), epigastric burning (21%), heartburn (14%-50%), postprandial fullness (14%), early satiety (14%), eructation (14%), regurgitation (7%-50%), or epigastric pain (7%). Evaluation of dysphagia in OA patients should begin with contrast studies that can be helpful in identifying a structural

etiology for dysphagia. Esophagography after OA repair should be performed because of the high index of suspicion for the presence of distal congenital esophageal stricture. Endoscopy with biopsies allows the evaluation of the anastomosis (stricture, diverticulum), the esophageal mucosa (peptic, eosinophilic or infectious esophagitis) and the diagnosis of congenital stenosis, mucosal bridge, inlet patch or extrinsic compression (vascular anomalies, tight fundoplication wrap) (Figure 1) [10,11].

Esophageal motility can be assessed by esophageal manometry. The patterns of esophageal dysmotility in a cohort of children with OA were recently described using high resolution manometry and were reported abnormal in all patients, with 3 types of abnormalities observed: pressurization (15%), isolated distal contractions (50%) and a peristalsis (35%) [12].The management of dysphagia must be conducted according to the underlying cause, such as feeding adaptation treatment of esophagitis (peptic, eosinophilic or infectious), prokinetics, surgical repair of vascular anomaly, gastrostomy tube feeding or dilation of fundoplication [10].

Gastroesophageal reflux and gastroesophageal reflux disease

Gastroesophageal reflux (GER) is the passage of gastric contents into the esophagus with or without regurgitation and vomiting. Repeated expulsion of gastroesophageal contents from the oral cavity in GER is reported to occur in approximately 40% of infants [7,13].

Gastroesophageal reflux disease (GERD) is present when the reflux of gastric contents causes troublesome symptoms and/or complications. The prevalence of symptomatic or pathologic GER or GERD is estimated to occur in 10% to 20% of infants in North America. Some children are at higher risk of GERD, including those with neurologic impairment, obesity, esophageal achalasia, hiatal hernia, prematurity, bronchopulmonary dysplasia, and OA. GERD can contribute to persistent dysphagia by reducing mucosal sensation and laryngeal reactivity during the pharyngeal phase of swallowing owing to mucosal injury by caustic reflex contents [7,13]. Coppens et al, confirmed the association of dysphagia with GERD, with or without fundoplication, in children with repaired OA. This is in accordance with previous research, which indicates abnormal oesophageal motility as common etiologic factor [9].

In infants and toddlers, there is no symptom or symptom complex that is diagnostic of GERD or predicts response to therapy. In older children and adolescents, as in adult patients, history and physical examination may be sufficient to diagnose GERD if the symptoms are typical. Complications of GERD are esophagitis, peptic stenosis and Barrett esophagus. The Combined Multiple Intraluminal Impedance and pH monitoring detects acid, weakly acid, and nonacid reflux episodes. It is the gold standard for GERD and is superior to pH monitoring alone for evaluation of the temporal relation between symptoms and GER. Esophageal manometry may be abnormal in patients with GERD but the findings arenot sufficiently sensitive or specific to confirm a diagnosis of GERD, nor to predict response to medical or surgical therapy. Endoscopically visible breaks in the distal esophageal mucosa are the most reliable evidence of reflux esophagitis. Endoscopic biopsy is important to identify or rule

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Table 1: Disorders commonly affecting feeding and swallowing in children.

Prematurity- Low gestational age at birth- Low birth weight- Comorbidities associated with prematurity

Congenital abnormalities-Tongue tie-Cleft lip/palate-Moebius syndrome-Down syndrome

Iatrogenic complications-Tube feeding-Tracheostomy-Respiratory support-Certain medications (especially those that affect arousal,awareness, muscle tone, or saliva production)

Gastrointestinal disorders- OA/TEF-GERD-EoE-Food allergies and intolerances-Achalasia-Congenital diaphragmatic hernia-Necrotizing enterocolitis-Hirschsprung disease-Gastroschisis

Respiratory and cardiac disorders-Apnea -Pulmonary dysplasia-Respiratory distress syndrome-Bronchopulmonary dysplasia -Laryngo-/tracheo-/bronchomalacia-Heart defects

Neuromuscular disorders-Microcephaly-Hydrocephalus-Intraventricular hemorrhage-Periventricularleukomalacia-Cerebral palsy-Seizures-Muscular dystrophy

Ingestional (caustic) injuries-Cleaning agents-Battery

Maternal and perinatal issues-Jaundice-Diabetes-Fetal alcohol syndrome-Neonatal abstinence syndrome

Abbreviations: OA: Oesophageal Atresia; TEF: Tracheo-Oesophageal Fistula; GERD: Gastroesophageal Reflux Disease; EoE: Eosinophilic Esophagitis

Figure 1 (a) Barium swallow of a symptomatic EoE stricture in OA–TEF patient. (b) EoE stricture in EA-TEF patient as seen endoscopically [Krishnan U. Eosinophilic Esophagitis in Children with Esophageal Atresia. Eur J Pediatr Surg. 2015; 25: 336-344].

Figure 2 Upper gastrointestinal study demonstrating a “bird’s beak” deformity (arrow) in a 17-year-old patient with achalasia. (Image provided by R. Ignacio 2016).

out other causes of esophagitis, and to diagnose and monitor Barrett esophagus and its complications [13].

The management of GERD includes dietary and lifestyle changes, medications (Histamine 2 receptor antagonists, Proton

pump inhibitors) and surgery with a Nissen fundoplication what may be performed on children at risk for life-threatening complications of GERD [14].

Eosinophilic esophagitis

Eosinophilic esophagitis (EoE) is a chronic immune-mediated condition characterized by clinical symptoms secondary to esophageal dysfunction and histologically by eosinophilic infiltration of the esophagus [15].

Clinical symptoms vary according to age. Feeding difficulties are the most common symptoms in infants and toddlers (including vomiting, regurgitation and feeding refusal). During childhood, vomiting and/or abdominal or retrosternal pain are reported, whereas during adolescence, GERD symptoms, dysphagia, and food impaction are the most frequent symptoms [7,15].

The consensus recommendation identified four dominant presenting symptoms of esophageal dysfunction: dysphagia, abdominal pain, GERD/vomiting, and failure to thrive/feeding difficulty [16].

Figure 3 Videofluoroscopy of a patient with dysphagia.

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The updated definition of the disease includes the histological presence of ≥15 eosinophils per high power field in at least 1 endoscopic esophageal mucosal biopsy (peak value) taken at upper gastrointestinal endoscopy; and/or the presence of other microscopic features of eosinophilic inflammation such as eosinophilic micro abscesses, superficial layering, or extracellular eosinophil granules [15]. EoE patients with dysphagia have significantly higher eosinophils compared to EoE patients with abdominal pain, and the level of inflammation as seen from eosinophil micro abscesses, superficial layering, desquamation, and the distribution around rete pegs is significantly higher [17].

Besides, recent studies suggest an increased incidence of EoE in OA–TEF patients. As presenting symptoms of EoE are similar to those of GERD, misdiagnosis or delayed diagnosis often occurs in OA patients, in whom anastomotic strictures, GERD, and dysphagia are common postoperatively[18,19]. Therefore, it is suggested that if these symptoms persist in patients with OA, performanupper digestive endoscopy with biopsies to rule out associated EoE [11].

The management consists of dietary modification and reflux therapy. Three diet forms are commonly prescribed: an elemental diet that is a liquid formula based on amino acids and free of all allergens, a 6-food elimination diet that removes commonly identified allergens, or a targeted elimination diet that eliminates food identified as allergic to patient after testing. Swallowed corticosteroids are also effective in treating acute exacerbations of EoE but the disease often relapses after discontinuation [15].

Achalasia

Achalasia is a rare esophageal neurodegenerative disorder characterized by failure of lower esophageal sphincter (LES) relaxation. The incidence of achalasia in childhood is 0.11/100000 children annually. The pathophysiologic basis of achalasia is characterized by the degeneration of the inhibitory my enteric plexus that innervates the LES and esophageal body. This leads to an imbalance in the inhibitory and excitatory neurons resulting in the failure of the LES to relax with swallowing, absence of peristalsis of the esophageal body, and increased LES resting pressures [20].

Children usually present with progressive dysphagia, vomiting, and weight loss. Younger children and infants may also present atypically with recurrent pneumonia, nocturnal cough, aspiration, hoarseness, and feeding difficulties [21].

Achalasia is diagnosed with a barium swallow study and may be confirmed with esophageal manometry. Barium swallow studies classically demonstrate a dilated esophagus with “bird’s-beak” like tapering of the distal esophagus (Figure 2). Elevated resting LES pressure, absent or low-amplitude peristalsis, or non-relaxing LES upon swallowing are diagnostic findings on esophageal manometry in children with achalasia. The various methods of treatment of achalasia involve reduction of LES pressure in order to facilitate esophageal emptying by: oral administration of calcium channel blockers, pneumatic dilatation, injection of botulinum toxin, esophageal myotomy with or without an anti-reflux procedure, and a novel technique called peroral endoscopic myotomy [20].

Cricopharyngeal achalasiaThe cricopharyngeus muscle is a striated muscle that is

contracted at rest, thus keeping the esophagus closed during respiration. Cricopharyngeal achalasia is thought to involve spasm or incomplete relaxation of the cricopharyngeus muscle. This is a rare cause of dysphagia in children and may develop between birth to 6 months of age. However, diagnosis may be delayed due to non-specific symptoms including choking, food regurgitation, nasal reflux, coughing recurrent pneumonia, cyanosis and failure to thrive [7, 22].

This disorder can be diagnosed by identification of a prominent bar on videofluoroscopic swallow study (VFSS) and increased pressures proximal to the muscle can also be demonstrated on manometry (Figure 3). The use of endoscopic dilatation is the first option because it is not an invasive technique, but it usually requires several sessions. The second-line therapy is surgery, a more aggressive technique. In addition, the injection of botulinum toxin represents a safe and effective alternative, although it is a less widespread method in pediatrics [7,23].

Assessment techniquesTechniques used for diagnosing and monitoring pediatric

dysphagia include clinical evaluation tools and quality of life measures, as well as a range of instrumental evaluation tools. VFSS and fiberoptic endoscopic evaluation of swallow (FEES) are the most commonly used instrumental assessments in pediatric dysphagia and they are considered gold standards in the diagnostic assessment of swallowing problems and aspiration [2,3] (Table).

VFSS allows for the assessment of the swallow in all of the swallowing stages. During this study, the patient is presented with barium-impregnated liquid and food, and video fluoroscopic monitoring is used to document oropharyngeal swallow function and swallowing disturbances [3]. In contrast to the VFSS, the FEES exam does not require intake of barium or radiation exposure, but it does require that a patient tolerate the passing of a nasal endoscope. FEES provides images of the larynx and hypopharynx before and after the pharyngeal swallow, which allows the detection of structural and physiological swallowing impairments, as well as an assessment of aspiration risk [24].

The upper gastrointestinal series (UGI) is a radiologic examination of the upper gastrointestinal tract and consists of a series of radiographic images delineating the esophagus, stomach, and duodenum. In the setting of dysphagia, a UGI can be helpful by noting anatomic and functional abnormalities, obstructions, as well as physiology of the oropharyngeal structures and UGI system. Esophagoscopy allows assessment and, if necessary, biopsies to identify GERD and EoE [1,7].

Other tools have received recent attention for their diagnostic usefulness as adjunct assessments for the diagnosis of dysphagia in pediatric populations, such as manometry and impedance. These tools provide information about pharyngeal and esophageal motility, as well as presence of Gastroesophageal reflux [3].

MANAGEMENTTherapy intervention for children with oral-phase swallowing

problems generally involves exercises aimed at improving the

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Ann Otolaryngol Rhinol 5(2): 1208 (2018) 5/5

sensory and/or motor skills required for drinking and eating. For children with swallowing problems affecting the pharyngeal phase, therapy intervention generally involves the child to modify their swallowing strategy or teaching the feeder to modify the bolus [3]. Furthermore, the treatment of dysphagia must be conducted according to the underlying cause.

CONCLUSIONChildren have rapidly developing body systems and even

short-term problems with swallowing can interrupt normal development and cause serious long-term sequelae.

Populations at particular risk of dysphagia include children with cerebral palsy, neuromuscular disorders, craniofacial malformations, congenital cardiac disease, children born preterm and children with gastrointestinal disease. The gastroesophageal causes of dysphagia should be suspected in order to make an approximation to the diagnosis and proper management.

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Karen Vanessa SS (2018) Dysphagia in Children: Gastroesophageal Causes. Ann Otolaryngol Rhinol 5(2): 1208.

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