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Meeting Organ forENT andPediatric
Pulmonology: Adenoids
ÇiğdemFiratKoca, CemalCingi, andSergeiKarpischenko
37.1 Introduction
The adenoid tissue is a lymphoid aggregate on the posterior and superior nasopharyngeal area [1]. The nasopharynx region is located at the posterior continuing of
nasal openings, where the inferior turbinate and the septum terminate. The soft palate
divides the oropharynx and nasopharynx. The Mucoperiosteum of the upper clivus
creates the structure of the nasopharyngeal roof. The mucosa, the prevertebral fascia,
the superior pharyngeal constrictor, and the longus capitis muscles comprise the
nasopharynx’s posterior side. The rear nasopharyngeal wall stands mid to clivus, the
anterior side of the foramen magnum, and the atlas. The orice of the Eustachian
tube exists in the lateral nasopharyngeal wall. The Rosenmüller fossa (pharyngeal
recess) is situated at the joint of lateral and posterior nasopharyngeal walls [2].
Adenoids are components of Waldeyer’s ring. Waldeyer’s ring, with its lymphoid nature, is formed by superiorly pharyngeal tonsils (adenoids), laterally two
palatine tonsils, inferiorly from the lingual tonsils, and located at the base of the
tongue [3]. Adenoid tissue development begins in the third month of fetal life.
Lymphocytes inltrate the glandular primordial situated in the posterior nasopharynx. Sagittal masses that create pharyngeal crypts appear in the fth month. The
surface of this formation is covered by pseudostratied ciliated columnar
37
Ç. F. Koca
Medical Faculty, Department of Otorhynolaryngology, Malatya Turgut Özal University,
Malatya, Turkey
C. Cingi (*)
Medical Faculty, Department of Otorhinolaryngology, Eskisehir Osmangazi University,
Eskişehir, Turkey
S. Karpischenko
Department of Otorhinolaryngology, The First Pavlov State Medical University of Saint
Petersburg, Saint Petersburg, Russia
© 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_37
475
476
epithelium, and the development of adenoids is completed in the seventh month of
fetal development [4]. The ascending pharyngeal artery, pharyngeal division of the
maxillary artery, and the cervical ascending arteries originating from the thyrocervical trunk provide blood supply to the adenoid tissue. Venous drainage is maintained via the pterygoid and pharyngeal to the internal jugular and facial veins.
Adenoid tissue is innervated with glossopharyngeal and branches of the vagus and
has no afferent lymphatics. Efferent lymphatic drainage is to the retropharyngeal
and upper cervical lymph nodes [4].
This chapter aimed to address adenoid and adenoid-related diseases and their
treatment modalities.
Ç. F. Koca et al.
37.2 Adenoid Hypertrophy
Adenoid hypertrophy is a frequent problem among pediatrics. When adenoid hypertrophy exceeds a certain level, lls the nasopharyngeal space, and extends the choana, it can cause upper-airway obstruction [1]. Adenoid tissue is small in the
neonatal period. It begins to grow in the rst years of life, reaches its maximum size
by age 5, and regresses after age 8 [5]. Chronic nasal obstruction due to adenoid
hypertrophy may cause symptoms include the following: hyponasality of voice,
obstructive sleep apnea (OSA), daytime sleepiness, behavioral and mouth breathing, snoring, attention problems, growth retardation, rhinorrhea, failure to thrive,
enuresis, and craniofacial issues. Severe obstructive sleep apnea may cause cor pulmonale with right heart failure [6].
37.3 Adenoid Hypertrophy andCraniofacial Development
The upper-airway obstruction due to enlarged adenoids may cause maxillofacial
dysfunctions [4]. The face shape that occurs due to chronic nasal obstruction due to
adenoid hypertrophy is the adenoid face. Adenoid face can be described as having a
short upper lip, a posterior positioned hyoid bone, a constricted upper dental arch, a
posterior position of mandibular incisors, an elongated anterior face, a constricted
or “V”-formed maxillary arc, a high mandibular plane angle, and a posterior positioned mandible [7]. Intraoral examination shows constricted maxillary and elevated palatal arcs and dental malocclusion [8].
Nasal obstruction may cause mouth breathing. Therefore, incisors face wetness
and get cold due to the vaporization. The mean results in pain, which initiates the
tongue-pushing reex to maintain optimal temperature for the incisors. Prolonged
breathing in the open-mouth position due to chronic obstruction induces the tonguepushing reex and anterior displacement of the tongue, and this chronic situation
may result in anterior open bite deformity [9]. Koca etal. detected a statistically
signicant elevation in the anterior face height and identied the posterior replacement of the mandible due to the hypertrophied adenoids. They also underlined the
importance of early intervention to the nasal obstruction in pediatrics to maintain
37 Meeting Organ forENT andPediatric Pulmonology: Adenoids
healthy dentofacial development [10]. Timing of adenoidectomy is critical to support the normal craniofacial development [7]. Average mandibular growth has been
claried after the adenoidectomy procedure with improved nasal breathing [8].
477
37.4 Adenoid Hypertrophy andPediatric Sleep
Breathing Disorders
Childhood OSA can be described as partial or complete obstruction of the upper
airway during sleep. Some associated symptoms are sleep disorders, hypercapnia,
hypoxemia, daytime sleepiness, snoring, enuresis, mouth breathing, and behavioral
and neurocognitive difculties. Enlarged adenoids alone, or with tonsil enlargement, are the most common predisposition factors for pediatric OSA due to nasopharyngeal and oropharyngeal obstruction. Adenoid tissue is a member of the
Waldeyer ring that completes its rapid growth between the ages of 2 and 8. Although
no direct relationship has been found between the thickness of adenoids and OSAS,
the OSAS clinic, considered an upper-airway motor or tonus disorder, causes
dynamic airway stenosis during sleep together with adenoid hypertrophy. Sleep disruption, fragmentation, hypoxia, and hypercapnia are some mechanisms accused of
neurocognitive and behavioral dysfunctions in pediatric sleep-disordered breathing
(SDB). Pediatric SDB may cause cardiac dysfunctions, blood pressure dysregulation, and growth retardation [11].
Intermittent hypoxia during sleep may inuence the neurochemical structure of
the brain and growth hormone secretion. Cardiovascular pathologies are associated
with increased intrathoracic pressure, excessive free circulating inammatory mediators, and increased insulin resistance. Pediatric OSA has been observed most frequently between the ages of 2 and 6 due to the largest size of adenoids. Adenoid
hypertrophy may cause obstructive problems, including nasal obstruction that
causes chronic mouth breathing, rhinorrhea, and dysphagia. Hypertrophy of adenoids due to an acute upper-respiratory system infection may lead to snoring and
nighttime breathing problems; this clinical period may end when the condition
improves, but this may be the onset of a challenging chronic upper-respiratory system obstruction [11]. Adenoid hypertrophy may cause neurocognitive changes,
including headache, daytime sleepiness, poor school performance, and learning difculties [5]. The mechanism of the neurobehavioral problems observed due to sleep
interruption is unclear. The possible tool is that sleep disruption and chronic hypoxia
may lead to functional impairments due to the alterations in the prefrontal cortex.
Low lingual visual capacity and poor school performance support that pediatrics
having hypertrophied adenoid tissue have difculties with their prefrontal cortex.
An essential academic improvement has been detected following adenoidectomy
[12, 13]. Koca et al. observed lower academic performance in the children with
hypertrophied adenoid tissue compared with the control group [10].
Sleep apnea requires a detailed examination by an ENT doctor and a sleep medicine
physician. It is critical to underline that OSA in children has different clinical features
from adults, as it is presented with more corrupted nocturnal sleep than excessive
478
daytime sleepiness and prominent behavioral disorders, including hyperactivity, enuresis nocturna, poor school performance, and psychiatric problems. Polysomnography
(PSG) is an accurate evaluation instrument that claries the obstructive events and
facilitates the classication of the severity of OSA.Enlargement of adenotonsillar tissue blocks the upper airway, and surgical intervention overcomes obstructive symptoms. Surgical procedure forms the rst treatment modality in OSA due to adenotonsillar
hypertrophy [14]. Adenoidectomy is a standard surgical procedure carried out alone or
combined with tonsillectomy for pediatric patients with OSA.A clinical study reported
adenoidectomy’s success in OSA treatment as 80% [4, 15, 16].
Ç. F. Koca et al.
37.5 Diagnosis ofAdenoid Hypertrophy
The nasopharynx is an anatomical location that is difcult to examine, with one end
extending from the base of the skull and the other to the soft palate. A small dental
mirror and a headlamp may help analyze the nasopharynx. A beroptic nasopharyngoscope is another alternative visualization method to maintain a perfect sight of the
nasopharyngeal area [17]. Posterior rhinoscopy and nasopharyngeal radiological
scans form the methods for evaluating adenoidal tissue. Flexible beroptic nasal
endoscopy is a popular, well-established, and commonly used procedure in otolaryngological practice, as it provides a perfect visualization and facilitates a correct
diagnosis to be performed. Nasal exible beroptic endoscopy is a safe method for
examining the nasopharyngeal region in children [18, 19]. Endoscopy provides a
direct visualization of nasal cavities and nasopharynx. Several techniques for grading enlarged adenoids have been published in the literature [18, 20]. The grading
system described by Parikh etal. (2006) has been most accepted for examining the
extension of adenoids over the posterior choanae; grade 1 for adenoids with no
contiguity with adjacent textures, grade 2 adenoids close contiguity with the torus
tuberous; grade 3 adenoids contiguity with the vomer and nally grade 4 adenoids
have close contiguity with the soft palate [21]. Lateral radiological examination of
the nasopharyngeal region has been carried out in pediatrics for many years to
determine the size of adenoid tissue. Paradise etal. reported that the radiograph was
in good accordance with the size of adenoids removed intraoperatively. Radiographs
are objective and noninvasive instruments for assessing the adenoidal size [22]. It is
not easy to perform this imaging modality for infants, and radiation exposure is a
disadvantage of the procedure that should not be neglected [23].
37.6 Surgical Indications forAdenoidectomy
1. Four or more attacks of recurrent purulent rhinorrhea in the previous 12-month
period in a child younger than 12.
2. Resistant complaints of adenoiditis despite antibiotic therapy (two courses of
therapy) (one antibiotic treatment period should be at least 14days and with a
beta-lactamase agent).
37 Meeting Organ forENT andPediatric Pulmonology: Adenoids
3. It prolonged sleep-related problems due to nasal blockage for at least 3months.
4. Hyponasality while speaking.
5. Serous otitis media persisting for longer than 3months period.
6. Dental malocclusion or orofacial developmental problems diagnosed by an
orthodontist.
7. Cor pulmonale, right ventricular hypertrophy, and pulmonary hypertension due
to upper-airway blockage.
8. Serous otitis media in the ages of 4 or older [24].
479
37.7 Preoperative Evaluation
Bleeding is the major complication of the adenoidectomy procedure. Bleeding diathesis of the medical and family history of the patient should be questioned in detail.
In suspicion of bleeding diathesis, a detailed hematologic evaluation is required. A
thorough otorhinolaryngological examination is essential in the presence of cleft
palate, submucous cleft palate, and velopharyngeal functions. Detection of bid
uvula should be reminded of the possibility of a submucous cleft palate. The atlantoaxial subluxation can be observed in pediatrics with Down syndrome. Before surgery in children with Down syndrome, the C1–2 joint should be examined with
cervical radiographs. Surgery can be performed in a neutral position in case of any
pathology.
37.8 Contraindications
The presence of bleeding diathesis creates a denite contraindication for adenoidectomy. The existence of a cleft palate may lead to postoperative velopharyngeal failure. A cleft palate is a contraindication for adenoidectomy due to the possibility of
postoperative velopharyngeal failure. Surgery should be avoided during poliomyelitis epidemics.
37.9 Complications
37.9.1 Bleeding
If the coagulation functions are standard in the patient, excessive bleeding is not
expected during the operation. Fibrosis due to recurring infections and active infections may cause bleeding. Adenoidectomy procedures can be carried out alone or in
combination with tonsillectomy. Bleeding prevalence has been reported between
0.1 and 58% after tonsillectomy and adenoidectomy. Bleeding in the postoperative
period is divided into early and late. Early period bleedings occur in the rst 24hours
after surgery. The most severe bleedings arise due to insufcient hemostasis during
the rst hour after surgery and are often noticed in the recovery room afterward.
480
First, the location of the bleeding should be determined. If the bleeding is severe and
the patient’s cooperation is difcult, intubation under general anesthesia should be
carried out to achieve appropriate hemostasis. Posterior packing can be placed to
control excessive bleeding. The posterior packing can be removed after 24–48h. A
blood transfusion may be required if the bleeding is severe, especially in children.
The most common cause of late-period bleedings, which occur in postoperative
5–7days, is infection. Late-period bleedings are treated in the same way.
Ç. F. Koca et al.
37.9.2 Hypernasality
Severe hypernasality incidence due to adenoidectomy and tonsillectomy has been
reported between 1/1500 and 1/10,000. Preoperative cleft palate or submucosal
cleft existence and velopharyngeal dysfunctions should alert the surgeon not to perform adenoidectomy. The patient is followed up for 3 months postoperatively.
Speech therapy should be started unless the compensation develops. Surgical intervention may be required in severe hypernasality. Bipolar cautery is recommended
for hemostasis intraoperative rather than unipolar cautery due to the harmful effect
of unipolar cautery on the nerves.
37.9.3 Surgical Traumas
The mouth opener can traumatize the tongue, lips, teeth, and temporomandibular
joint. Teeth can be detached, and the patient can aspirate these broken teeth. The
uvula, soft palate, and pharyngeal mucosa may be damaged. Burns may occur due
to cautery or laser devices used in the surgery.
37.9.4 Torticollis
Superior pharyngeal constrictor muscle may be traumatized while adenoid tissue is
curetted over the vertebrae in the posterior nasopharynx. Traumatization of the muscle may cause neck spasms, pain, and rarely torticollis. Grisel syndrome should be
suspected if neck movement limitation is accompanied by neck pain. Grisel’s syndrome can be described, as the nontraumatic subluxation or dislocation of the atlantoaxial joint or the C1 and C2 vertebrae. Warm compress, anti-inammatory
medication can be useful for resolving the spasm. Surgical treatment is rarely
required.
37.9.5 Otitis Media
Otitis media may occur after adenoidectomy surgery. Patients having otalgia following adenoidectomy should be evaluated by otoscopy.
37 Meeting Organ forENT andPediatric Pulmonology: Adenoids
481
37.9.6 Psychological Trauma
Surgical intervention may cause psychological trauma, particularly in pediatrics younger than 5. Sleep problems, behavioral disorders, and depression may
be observed in the postoperative period. Postoperative pain, young age, and
previous psychological problems can trigger postoperative behavioral disorders [25].
37.9.7 Nasopharyngeal Stenosis
An uncommon complication may be seen after a long period following the adenoidectomy procedure due to excessive mucosal destruction and infections [26]. Its
treatment is surgery.
37.9.8 Recurrence
Although it is rare, recurrence may be observed after adenoidectomies. The recurrence rate has been reported as 0.55% [27]. If adenoidectomy is performed young,
adenoid tissue can grow again during the child’s growth period.
37.10 Postoperative Care
After patients are discharged and sent home, close observation by their parents
should be recommended at home. Heavy physical activities are prohibited for
1–2weeks after surgery. Children can continue school a week later. A cold or warm
liquid diet is applied, particularly in the rst few days [4].
37.11 Surgery
Adenoidectomy is a frequent surgery carried out by otolaryngologists. The most
frequent indications are obstructive pathologies, including OSA, nasal obstruction,
recurrent OM, and otitis media with effusion. The classical transoral adenoidectomy method is performed with an adenoid curette or an adenectomy, usually under
general anesthesia. The surgery is always carried out without viewing the nasopharyngeal region. Classical transoral adenoidectomy may fail to achieve sufcient
removal of adenoids in one-third of cases, particularly when the existence of an
intranasal, superior, or peritubaric extension [28–33]. Complete removal of the
whole hypertrophied adenoids is the main aim of this procedure and suppresses the
recurrences. Digital control of the curetted area intraoperatively helps the surgeon
determine whether there is any rest tissue. Angle mirrors or endoscopic evaluation
are superior to directly visualizing the region [34]. With the endoscopic evaluation,