We greatly appreciate the help of Dr. Sara Arnold, MD, Medical College of Wisconsin, for allowing us to use the radiology pictures.
REFERENCES
1. Ganong W. Review of Medical Physiology. 22nd ed.
McGraw-Hill Medical; 2005:232.
2. Kleinman RE, Goulet OJ, Sanderson I, et al. Pediatric Gas- trointestinal Disease. BC Decker Inc.; 2008:128.
3. Richards CA, Milla PJ, Andrews PL, Spitz L. Retching and vomiting in neurologically impaired children after fun- doplication: predictive preoperative factors. J Pediatr Surg.
2001;36(9):1401–1404.
4. Granum PE, Lund T. Bacillus cereus and its food poison- ing toxins. FEMS Microbiol Lett. 1997;157(2):223–228.
5. Friedman JN, Goldman RD, Srivastava R, Parkin PC.
Development of a clinical dehydration scale for use in children between 1 and 36 months of age. J Pediatr.
2004;145(2):201–207.
6. Spergel JM, Brown-Whitehorn TF, Beausoleil JL, et al. 14 years of eosinophilic esophagitis: clinical features and prognosis. J Pediatr Gastroenterol Nutr. 2009;48(1):30–36.
7. Guarner J, Kalach N, Elitsur Y, Koletzko S. Helicobacter pylori diagnostic tests in children: review of the literature from 1999 to 2009. Eur J Pediatr. 2009: vol. 169(1):15-25.
8. Li BU. Cyclic vomiting: the pattern and syndrome paradigm.
J Pediatr Gastroenterol Nutr. 1995;21(suppl 1):S6–S10.
9. Kleinman RE, Goulet OJ, Sanderson I, et al. Pediatric Gas- trointestinal Disease. BC Decker Inc.; Hamilton, Ontario, Canada. 2008:129.
10. Li BU, Murray RD, Heitlinger LA, Robbins JL, Hayes JR.
Heterogeneity of diagnoses presenting as cyclic vomiting.
Pediatrics. 1998;102(3 Pt 1):583–587.
11. Tsai JD, Huang FY, Lin CC, et al. Intermittent hydroneph- rosis secondary to ureteropelvic junction obstruction:
clinical and imaging features. Pediatrics. 2006;117(1):
139–146.
12. Rudolph CD. Rudolph’s Pediatrics. 21st ed. McGraw-Hill;
2002:1351–1353.
13. Haans JJ, Masclee AA. Review article: the diagnosis and management of gastroparesis. Aliment Pharmacol Ther.
2007;26(suppl 2):37–46.
14. Apfel CC, Korttila K, Abdalla M, et al. A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med. 2004;350(24):2441–2451.
15. Kris MG, Hesketh PJ, Somerfi eld MR, et al. American Soci- ety of Clinical Oncology guideline for antiemetics in oncol- ogy: update 2006. J Clin Oncol. 2006;24(18):2932–2947.
16. Li BU, Lefevre F, Chelimsky GG, et al. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition consensus statement on the diagnosis and man- agement of cyclic vomiting syndrome. J Pediatr Gastroen- terol Nutr. 2008;47(3):379–393.
17. Li BU, Balint JP. Cyclic vomiting syndrome: evolution in our understanding of a brain–gut disorder. Adv Pediatr.
2000;47:117–160.
18. Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. N Engl J Med. 2006;354(16):1698.
19. Alhashimi D, Alhashimi H, Fedorowicz Z. Antiemetics for reducing vomiting related to acute gastroenteritis in chil- dren and adolescents. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD005506.
CHAPTER 3
Feeding and
Swallowing Disorders
Richard J. Noel
pathology (e.g. hypoplastic left heart syndrome).
Furthermore, feeding, the airway, and the upper gastro- intestinal tract exist in a reciprocal relationship system where problems with one of these components may produce problems in the others (Figure 3–1); such may be seen in an infant with pulmonary disease, where cough and tachypnea may aggravate refl ux and feeding problems, respectively. Additionally, the central nervous system, with respect both to basic motor and sensory function and to its higher order processes such as per- sonality development, exists in the background of this relationship and can both contribute to, and be affected by, problems of the airway, upper GI tract, and feeding ability (Figure 3–1).
PATHOGENESIS
Achievement of normal feeding is a function of skill acquisition as permitted by the child’s internal and external environments. The progression of feeding that
DEFINITIONS AND EPIDEMIOLOGY
Pediatric feeding disorders may be defi ned as problems with the developmentally appropriate intake of food.
This broad category includes diffi culties that objec- tively result in nutritional or medical risk (e.g., refusal of dietary protein leading to protein energy malnutri- tion), as well as those perceived as problematic by the child’s family that result in stressful mealtimes without objective medical consequence. These do not include eating disorders (i.e., anorexia and bulimia) or obesity.
Pediatric feeding disorders may be associated with medical disease (often gastrointestinal), malnutrition or failure to gain weight, developmental delays affect- ing skill acquisition, and interpersonal disorders. Feed- ing problems have been characterized simply along axes of ability and desire,1 by biophysical etiology,2 or by criteria that focus on interpersonal relationships.3 Children with feeding disorders are best assessed and managed by interdisciplinary teams that address all sides of the problem, given that distinct facets of the disorder require individual expert assessment and intervention.
Feeding disorders occur in children with an inci- dence as high as 25% in normal children,4 with a higher incidence in those with neurologic disability.5–7 While children with feeding disorders require evaluation by a gastroenterologist due to the high coincidence with gastrointestinal disorders,1,8 skill acquisition and behav- ioral components are often present and require behav- ioral evaluation and management beyond what a gastroenterologist may provide.9
An individual patient’s feeding disorder is unique.
Environmental and family social-dynamic issues are different for each individual with the same underlying
Feeding Airway
Upper GI tract
FIGURE 3–1 ■ Interplay between airway, gastrointestinal tract, and feeding ability. Feeding ability has a reciprocal relationship with the airway and the upper gastrointestinal tract, where one affects the others. In the background, the central nervous plays a role, in regard to both the motor and sensory function and the higher order personality and social dynamic issues.
occurs over infancy is governed by neuromuscular and anatomic maturation that limit the manner of feeding at any specifi c age.10 A newborn is limited by neurologic immaturity and unique anatomy that helps isolate the oral cavity from the airway. These limitations prevent the processing of solids, but maximize the effi ciency of suckling from a nipple. As the infant grows, the oral cav- ity enlarges and neuromuscular maturation occurs, manifested as lateral motion of the tongue, as well as improved head and truncal stability that allows the introduction of smooth solids. As the oral cavity grows, the larynx descends, and teeth appear, which together with further skill acquisition allow the introduction of more complex solids and table foods into the diet by 1 year of age. A strong element of social bonding drives the progression across feeding milestones, and infants learn to respond to positive reinforcement. Early expo- sure to various tastes may also play a role in fl avor pro- gramming and the later acceptance of a varied diet.11
Swallowing is a complex behavior that requires coordination of cranial nerves (V, VII, IX, X, and XII), cervical nerves (1 and 2), and corresponding sensory and motor endpoints to coordinate the oral and
pharyngeal phases (Table 3–1). Similar to data on abnormal visual cortex development associated with early onset blindness,12 children who miss developmen- tal “critical periods” in infancy often fail to progress across feeding milestones, presumably due to abnormal cortical development allowing coordination of swallow- ing function. Such a patient typically would not prog- ress across textures and may be subject to developing profound feeding disorders with possible social and/or medical consequences.
Interruption of this graded exposure and corre- sponding development occurs in many infants and chil- dren with congenital or transient disease states that interfere with progression of feeding skills. An infant with complex congenital heart disease may not be well enough to take initial oral feedings for several months after birth, resulting in a situation where graded food exposures have not occurred. This directly impairs neu- romuscular development, not to mention the social bonding that typically occurs with feeding. Recognition of such a feeding disorder is the fi rst step in properly addressing it and establishing realistic and developmen- tally appropriate expectations.
Table 6–1.
Innervation of Swallowing
Touch Taste
Oral phase
Afferent Trigeminal (V) Oral cavity, anterior
2/3 of tongue
None
Facial (VII) None Anterior 2/3 of tongue
Glossopharyngeal (IX) Posterior 1/3 of tongue Posterior 1/3 of tongue
Efferent Trigeminal (V) Muscles of mastication
Facial (VII) Lips and face
Vagus (X) Tongue
Hypoglossal (XII) C1 and C2 Pharyngeal phase
Afferent Glossopharyngeal (IX) Pharynx
Vagus (X) Larynx and esophagus
Efferent Trigeminal (V) Tensor veli palatini
Glossopharyngeal (IX) Palate, pharynx, larynx Vagus (X)
Trigeminal (V) Hyoid and laryngeal movement Facial (VII)
C1 and C2
Cranial nerves V, VII, IX, X, and XII and cervical spinal nerves 1 and 2 provide all motor and sensory information for the oral and the pharyngeal phases of swallowing.
Table 3–1.
will limit the progress that can be made over time. The family of a child who has already had a comprehensive multidisciplinary assessment that was negative may still believe a medical etiology is being missed. They may not be ready to address underlying interpersonal issues that are the likely etiology. Failure to both acknowledge and move beyond a family’s initial perceptions will result in inability to establish the trust required to guide the fam- ily through management of a feeding disorder.
It is common for children with feeding disorders to have had previous extensive medical evaluations, often at different institutions. Review of these medical records should be done prior to the clinic evaluation, sometimes with a limited telephone conversation with the family. This may be helpful in deciding which diag- nostic elements may be required, including videofl uo- roscopic swallow study (VSS), EGD, meal observations, or consultation and assessment with other subspecial- ists who are not routinely part of the team, such as neu- rology, genetics, or otolaryngology.
DIAGNOSIS
Diagnosis of a feeding disorder must include diagnosis of underlying and comorbid disorders. The former may include almost any pediatric disorder; the latter may include failure to gain weight, gastroesophageal refl ux disease (GERD), and dysphagia. Conceptually, the phy- sician leading the team must simultaneously evaluate three major issues: nutrition, upper GI tract dysfunc- tion, and dysphagia (Figure 3–2).