Sucking and Swallowing Disorders and Gastroesophageal Reflux
Colston F. McEvoy
Sucking and swallowing begin prenatally, with pharyngeal swallowing observed as early as 10 to 11 weeks’ gestation and suckling seen at 18 to 24 weeks. Late-term fetuses swallow amniotic fluid at a rate equal to that of fetal urination. Interruptions in fetal ingestion of amniotic fluid due to gastrointestinal tract obstruction or neurologic abnormalities can upset this balance and result in polyhydramnios.
Nonnutritive sucking is seen in premature infants at 27 to 28 weeks’ gestation and in the first 48 hours of life in term infants. This pattern is characterized by short bursts of one to five sucks with long pauses between. The number of sucks increases to 10 to 30 per burst in nutritive sucking, and these bursts become regularly associated with swallowing. In premature infants, a mature sucking pattern sufficient to support total oral intake of calories usually is achieved by 34 weeks’ gestation.
Coordination of sucking, swallowing, and breathing is a prerequisite to successful oral feeding. The anatomy of infants is such that a small oral cavity, a relatively large tongue, and an anteriorly and superiorly positioned larynx facilitate nasal breathing and airway protection. Early suckling progresses to true sucking in the older infant, with development of tighter lip approximation around the nipple and a progression from anteroposterior to vertical tongue motions. This progression allows for efficient delivery of liquid to the anterior chamber of the mouth. Swallowing is initiated when the tongue propels a liquid bolus backward into the pharynx. The soft palate closes off the palatopharyngeal isthmus, preventing liquid access to the nasopharynx. The tongue moves posteriorly against the pharyngeal wall while the larynx moves up, closing the epiglottis and preventing access to the airway. The pharyngeal constrictor muscles relax, followed by relaxation of the cricopharyngeus muscle or superior esophageal sphincter, and the bolus enters the upper esophagus. The tongue then moves away from the pharynx, and the epiglottis rises, allowing air into the trachea. Contraction of the cricopharyngeus muscle stimulates peristalsis, which carries the bolus to the distal esophagus. Relaxation of the lower esophageal sphincter permits entry into the stomach.
The causes of dysfunctional sucking and swallowing are varied (Box 57.1) and often result in poor growth due to inadequate oral intake and aspiration. Neuromuscular disease, usually characterized by hypotonia, may cause diminished suck or discoordinated swallow. Structural anomalies or lesions of the mouth, pharynx, or larynx often interfere with the mechanics of sucking and swallowing. At the level of the esophagus, congenital abnormalities, stricture, mucosal inflammation, or extrinsic compression may result in swallowing difficulty.
ACHALASIA
Achalasia is a motility disorder of the esophagus characterized by a functional obstruction of the esophagus. The characteristic findings are absent or nonperistaltic contractions of the esophagus, failure of the lower esophageal sphincter to relax with swallowing, and sometimes a high resting pressure of the lower esophageal sphincter. The estimated incidence in the general population is 1 in 100,000 per year. Only 5% of cases occur in children younger than 5 years of age. Allgrove or Triple A syndrome is an autosomal recessive disorder in which achalasia is associated with alacrima, adrenal insufficiency, and autonomic abnormalities. It often presents in childhood.
Children with achalasia have symptoms of vomiting, regurgitation, or dysphagia. Obstructive symptoms are first precipitated by solids, and as the disease progresses, the ability to swallow liquids may be affected or may be impaired. Affected children may have recurrent pulmonary infections, wheezing, and failure to thrive. An upper gastrointestinal examination may show characteristic “beaking” or tapering of the distal esophagus, with varying degrees of esophageal dilation (more prominent in older children than in the very young). The diagnosis is made by manometry, which shows failure or incomplete relaxation of the lower esophageal sphincter after swallowing, absent or disordered peristalsis, and elevated intraesophageal pressure. Treatment of achalasia consists of balloon dilation or surgical myotomy of the lower esophageal sphincter. Botulinum toxin injected into the lower esophageal sphincter temporarily relieves symptoms of obstruction. Chagas disease causes symptoms similar to those of idiopathic achalasia and is the result of esophageal neuronal damage by the parasite Trypanosoma cruzi. After surgical myotomy, gastroesophageal reflux may become a significant problem. Disordered esophageal peristalsis is a lifelong problem and may be the source of chronic symptoms of dysphagia.
GASTROESOPHAGEAL REFLUX
Gastroesophageal reflux (GER) is defined as the spontaneous regurgitation of gastric contents into the esophagus. Reflux occurs physiologically in young infants, the majority of whom have mild symptoms that resolve with age. GER is pathologic (GER disease) in infants who experience complications or in older children and adults. Mechanisms proposed for physiologic reflux include increased transient relaxation of the lower esophageal sphincter (LES), delayed gastric emptying, and an intraabdominal–LES pressure differential. Reduced resting LES pressure and esophageal dysmotility are often secondary results of acid damage to the esophagus in older children and adults but are rarely primary to the condition in infancy. In infants, the short esophagus, large meals in relation to gastric capacity, frequent feeding regimen, supine positioning, frequent Valsalva maneuver during the passage of stool while recumbent, and poorly developed swallowing response are all predisposing factors that improve with age.
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