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336
İ. B. Arslan and İ. Çukurova
Tonsillary Hypertrophy inChildren
25
AbdullahKınar, CemalCingi, andTaniaSih
25.1 Introduction
The palatine tonsils and adenoids are tissues of the Waldeyer ring, a group of lymphoepithelial tissues that includes tubal tonsils in the nasopharynx and the lingual
tonsil. Collectively, these tissues participate in the mucosal immune system of the
pharynx.
25.1.1 Waldeyer Ring
The German anatomist Heinrich von Waldeyer is noted for his anatomic description
of the lymphoid tissue in the posterior nasopharynx and oropharynx. As mentioned
previously, the Waldeyer ring consists of palatine (faucial) tonsils (the tonsils), pharyngeal tonsils (the adenoids), lingual tonsils, and tubal tonsils.
They are positioned strategically at the entrance of the gastrointestinal and respiratory tracts. The tonsils and adenoid serve as secondary lymphoid organs, initiating
immune responses against antigens entering the body through the mouth or
nose [1–4].
A. Kınar
Department of Otorhinolaryngology, Afyonkarahisar State Hospital, Afyonkarahisar, Turkey
C. Cingi (*)
Medical Faculty, Department of Otorhinolaryngology, Eskişehir Osmangazi University,
Eskisehir, Turkey
T. Sih
Department of Pediatric Otolaryngology, School of Medicine, University of São Paulo,
São Paulo, Brazil
e-mail: tsih@amcham.com.br
© 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_25
337
338
A. Kınar et al.
25.2 Embryology ofTonsils
During the fourth fetal month, epithelial crypts grow into the epithelial connective
tissue and are inltrated by lymphoid cells. In the fth month, the rst primary follicles are seen. The palatine tonsils are rst seen in the third month and are derived
from the ventral portion of the second pharyngeal pouch. During the fourth month,
ten solid epithelial (endodermal) buds entwine within the mesenchyme around the
pharyngeal wall, and canalization occurs via programmed cell death. By the third
trimester, organized lymph follicles are noted [1–4].
25.3 Anatomy
Palatine Tonsils Boundaries
• Anterior: Palatoglossus muscle.
• Posterior: Palatoglossus muscle.
• Lateral: Superior constrictor muscle.
Vascular Supply of Palatine Tonsils
• Tonsillar artery.
• Ascending pharyngeal artery.
• Tonsil branch of the facial artery.
• Dorsal lingual branch of the lingual artery.
• Ascending palatine branches of the facial artery.
Venous Drainage of Palatine Tonsils
• Peritonsillar plexus to the pharyngeal plexus, pterygoid plexus, and ultimately
into the internal jugular and facial veins.
A meaningful anatomic relationship to note surgically is that the internal carotid
artery is approximately 2.5cm posterolateral to the tonsil. The tonsil drains into the
tonsillar veins and the external palatine, pharyngeal, and facial veins. Another
important surgical note is that the palatine veins are the most common cause of
postoperative tonsillectomy bleeding.
25.3.1 Lymphatic Drainage
These are unique because they contain only efferent and no afferent lymphatic circulation; thus, lymph is not ltered through the tonsillar nodules. Drainage is
directly to jugulodigastric nodes, upper deep cervical lymph nodes, and indirectly
through retropharyngeal lymph nodes.
Efferent lymphatic drainage ows from the retropharyngeal lymph nodes to the
upper deep cervical lymph nodes, especially the posterior triangle nodes.
25 Tonsillary Hypertrophy inChildren
339
25.3.1.1 Nerve Supply
• Tonsillar branches of the maxillary nerve and glossopharyngeal nerve.
The glossopharyngeal nerve and styloid process descend almost vertically on
the lateral surface of this musculature. These tonsils are preserved via the
pterygopalatine (sphenopalatine) ganglion through the lesser palatine nerves
and from the glossopharyngeal nerve. Pediatric patients often complain of ear
pain after tonsillectomy.
This is referred to as pain via the glossopharyngeal nerve, which also supplies
the middle-ear cavity, including the medial wall of the tympanic membrane.
The blood supply to these tonsils includes the facial artery (tonsillar branch
and ascending palatine branch), ascending pharyngeal artery, dorsal lingual
branch of the lingual artery, and internal maxillary artery (descending palatine
artery, more signicant palatine artery) [2, 3].
25.4 Histology ofWaldeyer Ring
The epithelial covering of the palatine tonsils is stratied squamous epithelium,
which invaginates into the crypts. The palatine tonsils contain 10–20 crypts, which
penetrate the surface to reach various depths and may penetrate the entire tonsil to
reach the brous capsule and blends with the mesenchymal structures. Growth of
the palatine tonsils continues postnatally, and the palatine tonsil is active until age
15years [2].
After puberty, the tonsillar tissue tends to involute, and more brosis appears.
In contrast to other oronasal lymphoid tissues, the palatine tonsils are covered
with a pharynx basilar capsule fascia. The capsule is separated from the underlying
musculature by loose connective tissue. Pus can collect here and cause a peritonsillar abscess.
25.5 Immune Function ofWaldeyer Rings
The tonsils are the rst lymphoid aggregates to encounter pathogens that enter the
host via the upper respiratory and gastrointestinal tracts and thus are believed to
play a role in host immunity to pathogens.
Stimulation of the immune system begins shortly after birth [1–4]. Terminally
differentiated plasma cells can be seen around 2weeks of age. This results in the
development of secondary follicles. They also produce lymphocytes in a complete
sequence of lymphopoiesis and are related immunologically to the gut-associated
lymphoid system in humans [1–4].
Tonsils contain three other lymphoid compartments participating in immune
functions beneath the epithelium. The lymphoid follicles have two compartments:
the mantle zone and the germinal center (GC). The GC has a signicant B cell concentration and is the center of B-cell responses that include the clonal expansion of
B cells, the selection of B cells capable of receiving antigen-specic signals, the
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subsequent differentiation into B memory cells and plasma cells of various isotypes,
and the induction of the gene encoding the J-chain carbohydrate. The follicles also
contain a network of follicular dendritic cells (FDC) and a particular subset of germinal center dendritic cells that activate the GC T cells. The FDC can retain high
amounts of immune complexes on their plasma membranes for long periods and
thereby act as antigen-presenting cells, promoting the proliferation and differentiation of GC B cells [4].
The third or extrafollicular compartment contains T cells (primarily CD4+ helper
cells), interdigitating dendritic cells (IDC), macrophages, and high-endothelial
venules that facilitate the entry of T cells and B cells from the blood into the tonsils.
The region is also a center of cytokine and antibody production.
After passing through the crypt epithelium, M cells can initiate immunologic
responses, introducing foreign antigens to lymphocytes and antigen-presenting
cells (APCs).
Tonsils lack afferent lymphatics; however, the epithelium contains a system of
specialized channels lined by M cells that take up antigens into the vesicles and
transport them to the intra- and subepithelial spaces, where they are presented to
lymphoid cells. This transport function of M cells also serves as a portal for mucosal
infections and immunizations. In addition to their transport function, the M cells
initiate an immunologic response within the epithelium, bringing together high concentrations of foreign antigens with lymphocytes and antigen-presenting cells, such
as macrophages and dendritic cells.
After passing through the crypt epithelium, inhaled or ingested antigens reach
the extrafollicular region or lymphoid follicles. IDC and macrophages process the
antigens in the extrafollicular area and present them to CD4+ T lymphocytes. Helper
T cells then stimulate the proliferation of follicular B lymphocytes and their development into either antibody-expressing B memory cells capable of migration to the
nasopharynx and other sites or plasma cells that produce antibodies and release
them into the cryptlumen. Tonsillar plasma cells can have all ve immunoglobulin
(Ig) classes, helping to combat and prevent infection. Among the Ig isotypes, IgA
may be considered the most essential product of the adenotonsillar immune system.
In its dimeric form, IgA can attach to the transmembrane secretory component (SC)
to form secretory IgA (SIgA), a critical part of the mucosal immune system of the
upper airway. This component is necessary for binding IgA monomers to each other
and the SC and is an essential product of B cell activity in the tonsil follicles. While
the tonsils produce immunocytes bearing the J (joining) chain carbohydrate, the SC
is produced only in the adenoid and extra tonsillar epithelium, and therefore, only
the adenoid possesses a local secretory immune system [2–4].
25.6 Tonsillary Hypertrophy
The size of the tonsils appears to correlate with their level of immunologic activity,
peaking between the ages of 3 and 10years and demonstrating age-dependent involution. There is also some evidence that their size increases with bacterial load.
25 Tonsillary Hypertrophy inChildren
341
The tonsils and the adenoid are sites of continuous stimulation of the lymphoid
cells. The most excellent immunological activity of the tonsils is found between the
ages of 3 and 10years; the tonsils are most prominent during this childhood period
and subsequently demonstrate age-dependent involution. There is some evidence
that their size increases with the bacterial load and the population of B and T
cells [2–5].
At birth, the palatine tonsils are approximately 5mm in anteroposterior diameter
and 3.5mm in vertical diameter, weighing about 0.75g. During childhood, the palatine tonsils descend within their fossae as their vertical diameter grows faster than
their anteroposterior diameter. When lymphoid tissue occupies disproportionate
space in the pharynx, the upper airway becomes compromised.
Adenotonsillar disorders in children can be caused by various factors, including
pathogens, allergies, genetic predisposition, and, rarely, neoplastic proliferation.
Unilateral tonsillar hypertrophy should always raise suspicion of a tumor to physicians. Hyperplasia is a natural consequence of immune activity within these tissues
but may become problematic when tissue size becomes excessive for the pharyngeal space they occupy. Infection of the tonsils and adenoids is common in this age
group because they participate in immune processes and continuous exposure to
inhaled and ingested antigens [5–10].
In immunologic disorders like X-linked agammaglobulinemia (XLA; Brutontype agammaglobulinemia), it is a primary humoral immunodeciency characterized by recurrent bacterial infections of the respiratory tract and increased
susceptibility to enteroviral infection. The characteristic physical nding of XLA is
the absence, or near lack, of the tonsils and adenoids, although they may be present
if T cell areas are hypertrophied. The respiratory tract is the most common site of
bacterial infections in XLA [11].
Activation-induced cytidine deaminase (AID) deciency is a lack of lymphoid
and tonsillar tissue. Tonsillar hypertrophy is often prominent and may prompt tonsillectomy [11].
In Mucopolysaccharide storage disorders, thickening in the nose and pharynx
and hypertrophy of the tonsils and adenoids due to storage of glycosaminoglycans
(GAGs) in these tissues can be seen [7–10, 12, 13].
Feenstra B etal. identied and replicated a genetic association with the variant
rs2412971, intronic in HORMAD2at 22q12.2 with tonsillectomy. They also found
that the risk allele for tonsillectomy corresponded to an increased risk of IgA
nephropathy [14].
25.7 Physical Examination
Tonsil size is best determined in a neutral state (i.e., without the child gagging on a
tongue depressor) to accurately estimate the volume of the pharynx they occupy—
the Brodsky scale for clinical tonsil grading in children. Tonsil hyperplasia is graded
visually, most commonly using a scale of 1 to 4. Tonsillar size is often described on
a scale from 0 to 5 [15].
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A. Kınar et al.
• 0: Tonsils are entirely within the tonsillar pillar or previously removed by surgery.
• 1+: Tonsils occupy 0–25% of the posterior pharynx or tonsils hidden within ton-
sil pillars.
• 2+: Tonsils occupy 26–50% of the posterior pharynx or tonsils extending to the
pillars.
• 3+: Tonsils occupy 51–75% of the posterior pharynx or tonsils are beyond the
pillars.
• 4+: Tonsils occupy 76–100% of the posterior pharynx, or tonsils extend to the
midline. “Kissing tonsils” could be seen in severe hyperplasia.
25.8 Symptoms ofHyperplasia ofTonsils inChildhood
Obstructive sleep Apnea or sleep disturbances.
Failure to thrive.
Abnormal dentofacial growth.
Dental abnormalities.
Cardiac or pulmonary disease exacerbated by upper airway obstruction.
Eating or swallowing disorders.
Speech impairment.
Halitosis.
In children, hyperplasia of the tonsils and adenoids is commonly associated with
pharyngeal obstruction. During the daytime, children with an enlarged adenoid
demonstrate mouth breathing, rhinorrhea, and hyponasal speech, while those with
tonsil hyperplasia may exhibit a mufed, “hot potato” voice. However, the obstruction is even more apparent during sleep, when pharyngeal musculature relaxation
exacerbates airow resistance.
25.8.1 Obstructive Sleep Apnea
Obstructive sleep apnea is one of the most common reasons for adenotonsillectomyrelated adenotonsillar hypertrophy. Children with obesity (especially if severe) are
far more likely than lean children to have OSA, with reports of prevalence ranging
from 13% to 59% [16, 17].
Nocturnal Polysomnography PSG (overnight PSG) is considered the gold standard for diagnosis of OSA, as it is the only method able to denitively identify the
presence of obstructive events and quantify the severity of OSA, including gasexchange abnormalities and sleep disruption.
Obstructive sleep apnea increased in children <2years of age and children with
obesity (especially if severe), Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses obesity, achondroplasia, mucopolysaccharidoses, or craniofacial syndromes, or by dynamic
collapse such as occurs in the supine position and under conditions of diminished
25 Tonsillary Hypertrophy inChildren
343
neuromuscular tone such as sleep, Down syndrome, and cerebral palsy with prevalence estimates of 30–100% in Down syndrome, 15% in cerebral palsy, 85% in
Pierre-Robin sequence, and over 50% in children with achondroplasia [18–20].
Severity is generally quantied based on the obstructive apnea-hypopnea index
(OAHI). The OAHI is the total number of obstructive apneas and hypopneas divided
by the entire sleep duration in hours. Although there is no consensus on the denition of OSAS in children, an OAHI of ≤1 is considered within normal limits. An
OAHI of 1–5 is very mildly increased; 5–10 is mildly increased; 10–15 is moderately increased; and greater than 15 is severely abnormal. Unfortunately, polysomnography is expensive, time-consuming, and often unavailable. Other assessment
techniques, such as audiotaping, videotaping, and home and abbreviated polysomnography, may be helpful but must be more accurate.
Studies suggest that children with even mild OSAS demonstrate a morning blood
pressure surge, and those with OAHI greater than ve show increased blood pressure
load and 24-h ambulatory blood pressure, leading to cardiac hypertrophy. An association with enuresis has also been demonstrated in up to 50% of children with sleep
disturbances. The mechanism of this is not established, but theories include alterations in normal arousal and self-alerting mechanisms, hormonal changes (lower levels of antidiuretic hormone), and increased intra-abdominal pressure. In behavioral
studies, children with SRBD demonstrate signicantly higher prevalence rates of
problematic behaviors, including internalized (e.g., withdrawal, shyness, anxiety)
and externalized (e.g., emotional lability, impulsivity, hyperactivity, aggressiveness,
oppositional personality, somatic complaints, social problems) behaviors, compared
with controls. The strongest, most consistent associations are for externalizing,
hyperactive-type behaviors. Even children with primary snoring and OAHI less than
ve have been found to perform worse than controls on measures related to attention,
social problems, and anxious or depressive symptoms, as well as overall cognitive
abilities and some language and visuospatial functions. As a result, the polysomnographic level at which intervention should be considered for children with sleep disturbances and problem behaviors remains unclear. Neurocognitive impairment is
also noted in children with OSAS and appears more severe in children with OSAS
than in those with primary snoring. Several studies have established a lower level of
school performance among children with OSAS, and children with poor academic
performance are also more likely to demonstrate sleep disturbances [15, 21, 22].
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A. Kınar et al.
Halitosis DuetoPediatric Ear, Nose,
andThroat Field Infections
İlyasDişikırık and MahmutAlperKanmaz
26.1 Introduction
Halitosis is a general term used to describe the unpleasant odor in the breath due to
oral or non-oral reasons. It appears as a condition that can cause psychological
problems in children and their families. It has a multifactorial pathology. Although
it can occur due to intraoral and extraoral reasons, in 50% of patients in 90 cases,
the cause is intraoral [1].
Halitosis that originates from the mouth is called oral malodor [2]. It occurs due
to proteolytic destruction of organic substances in the mouth, especially by anaerobic bacteria found in the tongue coating [3]. Therefore, it is recommended to evaluate and reduce the microbial structure in the mouth in treatment [4].
The ssured structure of the tongue prepares the ground for bacteria to multiply
there [5, 6]. Thus, this ssured structure creates a basis for the proliferation and
growth of bacteria while also protecting these pathogens from the washing effect
of saliva.
The accumulation of food residues, epithelial residues, and bacteria on the
tongue dorsum as a coating is called tongue coating. It is stated that there is a close
relationship between tongue coating and lousy breath [3, 5]. For this reason, the
primary source of bad breath is accepted as the tongue dorsum [2, 3, 5].
Very few studies exist on the etiology and treatment of halitosis in children [7, 8].
Although halitosis occurs at different rates in different societies, the average
incidence is 5–33%.
26
İ. Dişikırık
Medical Faculty, Department of Otorhinolaryngology, Sanko University, Gaziantep, Turkey
M. A. Kanmaz (*)
Department of Otorhynolaryngology, Gaziantep Nizip State Hospital, Gaziantep, Turkey
© 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_26
345