Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
376
D. Barut et al.
Fig. 28.1 Algorithm for evaluation and management of pediatric dysphagia
not uniformly evaluated. Although they exist for certain disease groups, no validated dysphagia screening tests exist for children. Figure28.1 displays a strategy
for diagnosing and treating pediatric dysphagia. The objectives of the subsequent
tests include identifying a secure method of nutritional intake and the cause of the
dysphagia [7].
28 Dysphagia inChildren
377
28.5 Clinical Feeding Assessment
A speech-language pathologist (SLP) will frequently utilize a bedside swallow
examination as one of their initial methods of assessing a child who may have dysphagia. The patient is given a food bolus in this clinical test, and the clinician
watches the patient swallow. Only water is injected in some tests, while samples of
various consistencies could be tested in others. A progressive volume challenge or a
series of sips might introduce the water. The SLP can frequently identify whether
the dysfunction occurs during the preparation phase, oral phase, pharyngeal phase,
or a mixture of these phases. The SLP can determine the child’s participation ability
and the safety of continuing with more swallowing assessments. The bedside swallow is an adequate aspiration screening technique. However, it cannot pick up on
silent aspiration [19].
28.6 Fluoroscopic Swallow Study inVideo
The most popular test to assess patients with dysphagia is the videouoroscopic
swallow study, often known as the modied barium swallow study. The patient consumes food boluses ranging in viscosity from thin liquids to solids with infused
radiographic dye. When swallowing varied consistencies, uoroscopy checks for
any penetration or aspiration into the airway. To examine all four phases of swallowing, the child is placed as close to their natural feeding position as is physically
possible. This is done using a lateral radiography image. This procedure is the only
method that can denitively prove penetration and aspiration. This examination
cannot determine safe swallowing when nursing. The patient is exposed to radiation
during the videouoroscopic swallow study, and the time spent getting the test
increases the exposure to the youngster [8].
28.7 Flexible Endoscopic Swallowing Evaluation
Though some SLPs undertake this examination alone, an otolaryngologist and an
SLP typically perform a exible endoscopic evaluation of swallowing. Examining
the nasopharynx, oropharynx, hypopharynx, supraglottis, and glottis requires a exible nasopharyngoscope. This test gives the examiners a detailed analysis of the
patient’s upper aerodigestive tract anatomy. Then, food boluses are provided, and it
is possible to see them enter the airway as they are swallowed. The ability to analyze
a nursing infant and the lack of radiation exposure are two advantages of this evaluation. Complete swallows can be evaluated more than once without putting the
patient at greater risk. The inability to see the oral phase of swallowing, “white out”
during swallowing, where tissues contract and may obstruct that examination, the
failure to detect microaspiration, and the subjective nature of the evaluation are
some limitations of exible endoscopic evaluation of swallowing [7].
378
D. Barut et al.
28.8 Imaging
The upper gastrointestinal tract series involves a radiographic examination of the
esophagus, stomach, and duodenum while a food bolus impregnated with barium is
swallowed. This examination can assess the structural anatomy and the esophageal
swallowing phase. Chest radiography may be a crucial component of the workup in
children with concerns about recurrent aspiration or pneumonia. Chest radiography
could show signs of aspiration pneumonia or persistent lung disease. When choanal
atresia, micrognathia, and vascular anomalies are detected, computed tomography
or magnetic resonance imaging of the head, neck, and chest may also be recommended to assess suspected aberrant anatomy and further preoperative planning.
Additionally, the effects of chronic aspiration, such as bronchiectasis, can be shown
on chest computed tomography images.
28.9 Endoscopic Assessments
The comprehensive evaluation of a patient with pharyngeal or esophageal dysphagia and suspected penetration and aspiration must include direct laryngoscopy,
bronchoscopy, and esophagoscopy.
Endoscopies might not be necessary if oral dysphagia is isolated. The otolaryngology, pulmonology, and gastrointestinal teams can frequently coordinate the evaluations with the same surgical procedure. By employing the direct laryngoscopy
technique, the specialist in the eld of otolaryngology can assess the presence of
structural irregularities within several regions of the upper airway, including the oral
cavity, oropharynx, glottis, and subglottis. It is feasible to diagnose airway anomalies, including vallecular cysts, laryngomalacia, vocal fold immobility, and laryngotracheoesophageal aperture [20, 21].
Diagnoses for tracheomalacia, tracheal stenosis, and tracheoesophageal stula
can be made with a tracheoscopy. The bronchoscopy can check for bronchomalacia,
bronchiectasis, signs of persistent aspiration, and pneumonitis. The endoscopy can
be supplemented with further testing like biopsies, bronchial washing, pepsin, and
lipid-laden macrophage indices. An examination of the esophagus and, occasionally, distal tissues like the stomach and duodenum is possible during an esophagoscopy. It is possible to see mucosal alterations and extrinsic compression. To check
for eosinophilic esophagitis and GERD consequences, biopsies may be done. A
multichannel intraluminal impedance probe may be inserted to prevent acid and
nonacid reux [22].
28.9.1 High-Resolution Manometry
Esophageal dysphagia is a common complaint about referral for investigations of
esophageal motility after the exclusion of obstructive lesions by endoscopy and histology. High-resolution manometry (HRM) with esophageal pressure topography
28 Dysphagia inChildren
379
analysis is now the method for evaluating esophageal contractility [23]. In addition,
the dysfunction of bolus movement can lead to dysphagia, so evaluating bolus transit
is of great importance for a better understanding of esophageal dysphagia [24, 25].
HRM uses a solid-state catheter assembly with closely spaced pressure sensors
(typically 1-cm spacing intervals) positioned to traverse the entire length of the
esophagus. Software interpolating this pressure data to esophageal pressure topography (EPT) allows visualization of esophageal motor function along a space-timepressure continuum. In addition, the development of esophageal pressure topography
(EPT) metrics aimed to provide a quantitative assessment of many aspects of esophageal motor function. These metrics include the measurement of deglutitive loweresophageal sphincter (LES) relaxation using the integrated relaxation pressure
(IRP) and the evaluation of peristaltic vigor using the distal contractile integral
(DCI) [26, 27]. These EPT metrics and recognition of pressurization patterns on
EPT facilitated the development of a hierarchical classication scheme of esophageal motility disorders: the Chicago Classication [28]. The Chicago classication
provides a standard terminology for describing esophageal motility disorders and is
used worldwide.
28.10 Medical Management
The care of a multidisciplinary team with expertise in pediatric swallowing difculties is benecial for children with dysphagia. Pediatricians, developmental pediatricians, neurologists, otolaryngologists, pulmonologists, and gastroenterologists
could make up this team. When no other abnormalities are discovered during a
thorough examination, including endoscopies, children with dysphagia should
receive special consideration from a neurologic specialist. Accurately identifying
the underlying etiology is crucial for effectively managing dysphagia [3, 12, 29].
Feeding therapy, performed by an experienced SLP, is often the rst-line treatment for infants and children with dysphagia. To improve the suck-swallow-breathe
sequence, this therapy may involve adjusting the method of food delivery, such as
the nipple ow or spoon, feeding position, or feeding pace. The strength, mobility,
and coordination of the lips, tongue, jaw, soft palate, and pharyngeal muscles are
enhanced by sensory and motor exercises administered by a certied speechlanguage pathologist. Only if it is determined that the child is safe to try oral intake
may feeding treatment be tried [3, 29].
A study may also test other formulations to see if the patient tolerates them better. The nutritional value of feeds may be improved by increasing their caloric
content if a child can consume some oral meals. It might be essential to consult a
pediatric dietitian to maintain proper nutritional intake. If modifying the formula
doesn’t work, the food bolus’ consistency may need to be thickened. Thickened
feeds might lessen or treat GERD, aspiration, and laryngeal penetration. By
decreasing bolus transit and enhancing bolus cohesiveness during a swallow, thickeners have also been proven to alter swallowing mechanics and improve feeding
pacing [29, 30].
380
Based on GERD clinical symptoms, reux regimens, such as proton pump inhibitors and histamine H2 receptor antagonists, are frequently given. Numerous dysphagia symptoms resemble GERD symptoms, leading to the misuse of
pharmaceutical treatment. In 1–2years, many infants with aspiration will improve
with time and prudent management [31, 32].
D. Barut et al.
28.11 Surgical Management
The surgical treatment of dysphagia in pediatric patients is recommended when a
structural anomaly is determined to be the underlying cause of the swallowing
difculty.
28.11.1 Ankyloglossia
Ankyloglossia, commonly referred to as tongue-tie, is a subject that has garnered
signicant attention and generated considerable debate within the eld of feeding
research. Frenotomy refers to the surgical procedure involving the division of the
lingual frenulum and improves feeding in many patients with ankyloglossia and
restricted tongue range of motion. The surgery is often associated with a low level
of risk, with rare occurrences of problems such as bleeding, infection, harm to the
salivary ducts, and the potential necessity for correction. Nevertheless, there is an
increasing apprehension regarding the potential overdiagnosis and overtreatment of
ankyloglossia. A constricted lingual frenulum is frequently recognized as contributing to breastfeeding challenges. However, it is essential to acknowledge that the
underlying issue is typically more complex, involving various factors such as the
positioning of the jaw, the characteristics of the maternal nipple, and the coordination of oral movements [33].
28.11.2 Laryngomalacia
Laryngomalacia is a medical condition characterized by the abnormal softening
of the tissues. The presence of swallowing difculty in individuals with laryngomalacia is believed to be caused by multiple factors. The prevalence of dysphagia in individuals diagnosed with laryngomalacia has been documented to
range from 50% to 86%, regardless of any additional medical comorbidities.
The disability could be associated with reduced sensory perception and neuromuscular control of the pharynx and larynx inherent to laryngomalacia. The
physically restricted larynx imposes a more signicant workload on breathing
during feeding, disrupting the typical sequence of suck-swallow-breathe.
Supraglottoplasty is a microlaryngeal procedure that divides the aryepiglottic
folds and removes redundant supra- arytenoid tissue using cold steel, laser, or
microdebride [34, 35].
28 Dysphagia inChildren
381
28.11.3 Laryngeal Cleft
The laryngeal cleft is another area of signicant study and controversy in the otolaryngology literature. The condition known as laryngeal cleft can be classied into
four distinct degrees based on the extent of the interarytenoid cleft. Type 1 involves
an extension of the cleft up to the level of the vocal folds, while type 2 extends
beyond the vocal folds and into the cricoid cartilage. Type 3 is characterized by an
extension of the aperture into the cervical trachea, and type 4 involves an extension
into the thoracic trachea. The prevailing consensus in the eld acknowledges that
cleft types 2–4 are classied as anatomical anomalies and necessitate surgical intervention for healing. The laryngeal cleft is diagnosed on direct laryngoscopy with
palpation of the interarytenoid groove [36].
28.12 Conclusions
Dysphagia is a disease that is becoming more prevalent among pediatric patients,
mainly due to advancements in healthcare that have led to increased survival rates
among premature and medically complicated children. Dysphagia can arise from
diverse causes, frequently exhibiting a multifactorial nature. Utilizing a multidisciplinary team for evaluation purposes can enhance the precision of diagnoses and
provide valuable guidance for effective management strategies.
References
1. Gosa MM, Carden HT, Jacks CC, Threadgill AY, Sidlovsky TC.Evidence to support treatment
options for children with swallowing and feeding disorders: a systematic review. J Pediatr
Rehabil Med. 2017;10:107–36.
2. Dodrill P, Gosa MM.Pediatric dysphagia: physiology, assessment, and management. Ann Nutr
Metab. 2015;66:24–31.
3. Kakodkar K, Schroeder JW Jr. Pediatric dysphagia. Pediatr Clin N Am. 2013;60:969–77.
4. Bhattacharyya N.The prevalence of pediatric voice and swallowing problems in the United
States. Laryngoscope. 2015;125:746–50.
5. Benfer KA, Weir KA, Bell KL, Ware RS, Davies PS, Boyd RN. Oropharyngeal dysphagia in preschool children with cerebral palsy: oral phase impairments. Res Dev Disabil.
2014;35:3469–81.
6. Raol N, Schrepfer T, Hartnick C. Aspiration and dysphagia in the neonatal patient. Clin
Perinatol. 2018;45(4):645–60. https://doi.org/10.1016/j.clp.2018.07.005.
7. Durvasula VSPB, O’Neill AC, Richter GT. Oropharyngeal dysphagia in children: mechanism, source, and management. Otolaryngol Clin North Am. 2014;47(5):691–720. https://doi.
org/10.1016/j.otc.2014.06.004.
8. Delaney AL, Arvedson JC.Development of swallowing and feeding: prenatal through the rst
year of life. Dev Disabil Res Rev. 2008;14(2):105–17. https://doi.org/10.1002/ddrr.16.
9. McFarland DH, Lund JP.Modication of mastication and respiration during swallowing in the
adult human. J Neurophysiol. 1995;74(4):1509–17. https://doi.org/10.1152/jn.1995.74.4.1509.
10. Miller CK, Willging JP. Advances in the evaluation and management of pediatric dysphagia. Curr Opin Otolaryngol Head Neck Surg. 2003;11(6):442–6. https://doi.
org/10.1097/00020840- 200312000- 00006.
382
11. Motion S, Northstone K, Emond A, etal. Persistent early feeding difculties and subsequent
growth and developmental outcomes. Ambul Child Health. 2001;7(3/4):231–7. https://doi.
org/10.1046/j.1467- 0658.2001.00139.x.
12. Durvasula VSPB, Lawson BR, Bower CM, Richter GT. Supraglottoplasty outcomes in
neurologically affected and syndromic children. JAMA Otolaryngol Head Neck Surg.
2014;140(8):704–11. https://doi.org/10.1001/jamaoto.2014.983.
13. Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric gastroesophageal reux clinical
practice guidelines: joint recommendations of the North American Society for Pediatric
Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric
Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2018;66(3):516–54.
https://doi.org/10.1097/MPG.0000000000001889.
14. Noel RJ, Putnam PE, Rothenberg ME. Eosinophilic esophagitis. N Engl J Med.
2004;351(9):940–1. https://doi.org/10.1056/NEJM200408263510924.
15. Mohan S, Bowe SN, Hirner LM, Zar-Kessler C, Hartnick CJ.Modied approach for pediatric
external cricopharyngeal myotomy. Int J Pediatr Otorhinolaryngol. 2018;105:111–4. https://
doi.org/10.1016/j.ijporl.2017.12.019.
16. Malkar MB, Jadcherla S. Neuromotor mechanisms of pharyngoesophageal motility in dysphagic infants with congenital heart disease. Pediatr Res. 2014;76(2):190–6. https://doi.
org/10.1038/1- pr.2014.68.
17. Duncan DR, Mitchell PD, Larson K, Rosen RL. Presenting signs and symptoms do not
predict aspiration risk in children. J Pediatr. 2018;201:141–6. https://doi.org/10.1016/j.
jpeds.2018.05.030.
18. Velayutham P, Irace AL, Kawai K, et al. Silent aspiration: who is at risk? Laryngoscope.
2018;128(8):1952–7. https://doi.org/10.1002/lary.27070.
19. Brodsky MB, Suiter DM, González-Fernández M, et al. Screening accuracy for aspiration using bedside water swallow tests: a systematic review and meta-analysis. Chest.
2016;150(1):148–63. https://doi.org/10.1016/j.chest.2016.03.059.
20. Irace AL, Dombrowski ND, Kawai K, etal. Aspiration in children with unilateral vocal fold
paralysis. Laryngoscope. 2019;129(3):569–73. https://doi.org/10.1002/lary.27410.
21. Irace AL, Dombrowski ND, Kawai K, et al. Evaluation of aspiration in infants with laryngomalacia and recurrent respiratory and feeding difculties. JAMA Otolaryngol Head Neck
Surg. 2019;145(2):146–51. https://doi.org/10.1001/jamaoto.2018.3642.
22. Kieran SM, Katz E, Rosen R, Khatwa U, Martin T, Rahbar R. The lipid-laden macrophage
index as a marker of aspiration in patients with type I and II laryngeal clefts. Int J Pediatr
Otorhinolaryngol. 2010;74(7):743–6. https://doi.org/10.1016/j.ijporl.2010.03.028.
23. Fox MR, Bredenoord AJ.Oesophageal high-resolution manometry: moving from research into
clinical practice. Gut. 2008;57:405–23.
24. Srinivasan R, Vela MF, Katz PO, etal. Esophageal function testing using multichannel intraluminal impedance. Am J Physiol Gastrointest Liver Physiol. 2001;280:G457–62.
25. Fass J, Silny J, Braun J, etal. Measuring esophageal motility with a new intraluminal impedance device. First clinical results in reux patients. Scand J Gastroenterol. 1994;29:693–702.
26. Ghosh SK, Pandolno JE, Zhang Q, etal. Quantifying esophageal peristalsis with high-resolution manometry: a study of asymptomatic volunteers. Am J Physiol Gastrointest Liver Physiol.
2006;290(5):G988–97. [PubMed: 16410365]
27. Ghosh SK, Pandolno JE, Rice J, et al. Impaired deglutitive EGJ relaxation in clinical
esophageal manometry: a quantitative analysis of 400 patients and 75 controls. Am J Physiol
Gastrointest Liver Physiol. 2007;293(4):G878–85. [PubMed: 1769012]
28. Pandolno JE, Ghosh SK, Rice J, etal. Classifying esophageal motility by pressure topography
characteristics: a study of 400 patients and 75 controls. Am J Gastroenterol. 2008;103(1):27–37.
[PubMed: 17900331]
29. Borowitz KC, Borowitz SM.Feeding problems in infants and children: assessment and etiology. Pediatr Clin N Am. 2018;65(1):59–72. https://doi.org/10.1016/j.pcl.2017.08.021.
30. Duncan DR, Larson K, Rosen RL.Clinical aspects of thickeners for pediatric gastroesophageal reux and oropharyngeal dysphagia. Curr Gastroenterol Rep. 2019;21(7):30. https://doi.
org/10.1007/s11894- 019- 0697- 2.
D. Barut et al.
28 Dysphagia inChildren
31. Duncan DR, Amirault J, Johnston N, Mitchell P, Larson K, Rosen RL.Gastroesophageal reux
burden, even in children that aspirate, does not increase pediatric hospitalization. J Pediatr
Gastroenterol Nutr. 2016;63(2):210–7. https://doi.org/10.1097/MPG.0000000000001092.
32. Casazza GC, Graham ME, Asfour F, O’Gorman M, Skirko J, Meier JD.Aspiration in the otherwise healthy infant—is there a natural course for improvement? [published online March 5,
2019]. Laryngoscope. 2019;130:514–20. https://doi.org/10.1002/lary.27888.
33. Walsh J, McKenna Benoit M. Ankyloglossia and other oral ties. Otolaryngol Clin N Am.
2019;52(5):795–811. https://doi.org/10.1016/j.otc.2019.06.008.
34. Simons JP, Greenberg LL, Mehta DK, Fabio A, Maguire RC, Mandell DL.Laryngomalacia and
swallowing function in children. Laryngoscope. 2016;126(2):478–84. https://doi.org/10.1002/
lary.25440.
35. Scott BL, Lam D, MacArthur C. Laryngomalacia and swallow dysfunction. [published online May 23, 2019]. Ear Nose Throat J. 2019;98(10):613–6. https://doi.
org/10.1177/0145561319847459.
36. Johnston DR, Watters K, Ferrari LR, Rahbar R.Laryngeal cleft: evaluation and management. Int
J Pediatr Otorhinolaryngol. 2014;78(6):905–11. https://doi.org/10.1016/j.ijporl.2014.03.015.
383
Cervical Lymphadenopathy inChildren
29
MehmetKantar andEdaAtaseven
29.1 Introduction
Cervical lymphadenopathy is one of the most common complaints for hospital
referral in children. In many cases, children have benign cervical lymph node
enlargements as an immune response to viral or bacterial infections, or vaccines.
Less common reasons are pathological conditions such as suppurative lymphadenitis, granulomatous lymphadenitis, malignancies, Langerhans cell histiocytosis,
Rosai-Dorfman disease, and Castleman’s disease that require further investigation.
Besides acute suppurative lymphadenitis, children may undergo surgical excision to
determine possible pathology. In a systematic review of pediatric cervical lymphadenopathy, nonspecic benign etiology is present in 67.8% while Epstein-Barr
virus in 8.86%, malignancy 4.69%, and granulomatous disease 4.06% [1].
In this section, frequent causes of lymphadenopathy in children are summarized.
29.2 Reactive Lymph Node Enlargements
Lymph nodes are immune surveillance points of the immune system. Afferent lymphatics bring antigen-loaded dendritic cells to the lymph node, and they present
their antigens to T cells in the paracortical areas of the lymph node. Then, T cells
begin to differentiate and proliferate. T cells stimulate B cells, and then they become
plasma cells to secrete antibodies. Later, CD4+ and CD8+ effector cells and antibody reach the inammation-infection site via effect lymphatics and blood
circulation.
M. Kantar (*) · E. Ataseven
Division of Pediatric Hematology-Oncology, Department of Pediatrics, Ege University
School of Medicine, Izmir, Turkey
e-mail: mehmet.kantar@ege.edu.tr
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_29
385
386
This lymphoproliferation (functional hyperplasia) and stromal growth result in
lymph node enlargement (1–3cm). After inammation and infection resolve, cell
count returns to normal, but stromal shrinkage takes weeks. Therefore, reactive
enlarged lymph nodes regress and disappear slowly. These lymph nodes are palpated as soft, nontender, and elastic in consistency. Antibiotic use in this situation is
unnecessary because this is a normal immune reaction.
M. Kantar and E. Ataseven
29.3 Vaccines
Immune cells in the lymph nodes proliferate when exposed to the vaccine antigens.
Cervical as well as axillary lymphadenopathy are reported after measles, inuenza,
BCG, HPV, meningococci, and Covid-19 vaccines [2, 3]. Recently in Covid-19 vac-
cination, lymphadenopathy seems to be a reaction common to most vaccines rather
than specically to those of COVID-19. Hence, the mechanism in which lymphadenopathy occurs may be similar in all vaccine types [2].
29.4 Acute Suppurative Lymphadenitis
Suppurative lymphadenitis, secondary to a bacterial infection, is the major cause of
cervical lymphadenopathy in the pediatric population. Acute bacterial lymphadenitis predominantly affects healthy preschool-aged children and infants [4]. Acute
inammatory reactions are typically the outcome of pyogenic microorganisms
involving lymph nodes [5]. Most cases of acute bacterial lymphadenitis are due to
Staphylococcus aureus or Streptococcus pyogenes. However, group B streptococcal
lymphadenitis may present in infants. Anaerobic bacteria can occur, especially, in
older children with periodontal diseases.
The diagnosis of acute bacterial lymphadenitis depends on the physical examination and the patient’s medical history. Patients typically present with a history of
fever, sore throat, or cough, and physical ndings of pharyngitis, tonsillitis, and
acute otitis media. The timing of onset will be days to a week, with fever and an
enlarging neck swelling. On physical examination, lymph nodes may be rm and
tender with overlying erythema, and the neck range of motion may be limited [6].
Fluctuance develops in 25% of patients with acute bacterial lymphadenitis as a
sign of abscess formation. When differentiating between viral and bacterial lymphadenitis, it is essential to remember that viral lymphadenitis self-resolves. If the
patient does not begin to show resolution of infection within 4–7days, the clinician
should become concerned about either primary bacterial lymphadenitis or viral
lymphadenitis infected with bacteria.
The treatment for acute bacterial cervical lymphadenitis starts with appropriate
antibiotics. Patients can be given oral medications such as amoxicillin/clavulanate,
cephalosporins, clindamycin, or macrolides that cover the most frequent infections.
In order to begin parenteral antibiotic therapy, patients with severe symptoms may
need to be admitted to the hospital. The usual regimen begins with clindamycin or
ampicillin/sulbactam [7]. If large uctuant or persistent cervical lymphadenitis does
not respond to antibiotic treatment within 2–3days, the clinician should consider