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O. Oğuz et al.
opposes that of the lateral cricoarytenoid muscles. The posterior cricoarytenoid
muscles receive innervation from the recurrent laryngeal branch of the vagus nerve
(CN X) [9].
Lateral Cricoarytenoid Muscles
The lateral cricoarytenoid muscle on each side extends from the upper border of the
arch of the cricoid cartilage to the muscular process of the arytenoid cartilage on the
same side. These muscles function to rotate the arytenoid cartilages medially,
thereby adducting the vocal cords. The lateral cricoarytenoid muscles receive innervation from the recurrent laryngeal branch of the vagus nerve (CN X) [9].
Transverse Arytenoid Muscle
The transverse arytenoid muscle is a single muscle that extends between the posterior surfaces of each arytenoid cartilage. Its main function is the adduction of the
vocal cords, and it is innervated by both recurrent laryngeal branches of the vagus
nerves (CN X) [9].
Thyroarytenoid Muscles
The thyroarytenoid muscles run from a vertical line on the interior surface of the
thyroid cartilage angle and adjacent to the external surface of the cricothyroid ligament to the anterolateral surface of the arytenoid cartilage. Each muscle consists of
two parts: the vocalis and thyroepiglottic part [9].
The vocalis part lies deep and inferior, parallel with the vocal ligament to which
it is attached at the posterior end. The thyroepiglottic part is occasionally described
as a separate muscle; it lies superior and continues into the aryepiglottic fold, where
some bers extend to the margin of the epiglottis. These muscles function to draw
the arytenoid cartilages forward, thereby relaxing and shortening the vocal cords,
while also rotating the arytenoid cartilages inward, thus adducting the vocal folds
and narrowing the rima glottis. The thyroarytenoid muscles receive innervation
from the recurrent laryngeal branch of the vagus nerve (CN X) [9].
3.2.1.5 Nerves oftheLarynx
Superior Laryngeal Nerve
The superior laryngeal nerves arise from the inferior ganglia of the vagus nerve and
receive a branch from the superior cervical sympathetic ganglion on each side of the
upper neck. They descend adjacent to the pharynx on either side, behind the internal
carotid artery, and divide into internal and external branches [9].
The external branch (external laryngeal nerve) descends beneath the sternothyroid muscle and supplies the cricothyroid muscle. Injury to this nerve during thyroidectomy or cricothyrotomy causes hoarseness of the voice and an inability to
produce high-pitched sounds [9].
The internal branch (internal laryngeal nerve) pierces the thyrohyoid membrane
and supplies sensory innervation to the laryngeal cavity down to the level of the
vocal folds. It is responsible for the cough reex [9].
3 Structural andPhysiological Basis oftheUpper Respiratory Tract
43
Recurrent Laryngeal Branch oftheVagus Nerve (CN X)
The recurrent laryngeal branches of the vagus nerves ascend into the larynx within
the groove between the esophagus and the trachea. The left recurrent laryngeal
nerve originates in the thorax, looping under the aortic arch before ascending, while
the right recurrent laryngeal nerve originates in the neck [9].
These nerves are responsible for supplying sensory innervation to the laryngeal
cavity below the level of the vocal folds, as well as motor innervation to all laryngeal muscles except the cricothyroid. Since the nerves run immediately posterior to
the thyroid gland, they are at risk of injury during thyroidectomies. Unilateral nerve
damage presents with voice changes, including hoarseness. Bilateral nerve damage
may result in aphonia (inability to speak) and breathing difculties [9].
3.2.1.6 Vessels oftheLarynx
Arteries
The superior and inferior laryngeal arteries supply the majority of blood to the larynx. The superior laryngeal artery originates from the superior thyroid branch of the
external carotid artery and enters the larynx with the internal branch of the superior
laryngeal nerve through the lateral aperture of the thyrohyoid membrane. The inferior laryngeal artery originates from the inferior thyroid branch of the thyrocervical
trunk, which is a branch of the subclavian artery. It ascends into the larynx within
the groove between the esophagus and the trachea, along with the recurrent laryngeal branch of the vagus nerve (CN X) [9].
Veins
The superior and inferior laryngeal veins drain the larynx and share the same
course as the arteries. The superior laryngeal veins drain into the superior thyroid
veins, which empty into the internal jugular veins. The inferior laryngeal veins
drain into the inferior thyroid veins, which both empty into the left brachiocephalic
vein [9].
Lymphatics
The lymphatic vessels that drain above the vocal folds travel along the superior
laryngeal artery and drain to the deep cervical lymph nodes at the bifurcation of the
common carotid artery. The lymphatic vessels that drain below the vocal folds travel
along the inferior thyroid artery and drain to the upper tracheal lymph nodes [9].
3.2.1.7 Functional Anatomy oftheLarynx
Swallowing
During swallowing, the rima glottidis, rima vestibuli, and vestibule are closed. The
backward motion of the tongue forces the epiglottis over the opening of the glottis
to cover the laryngeal inlet and prevent aspiration of swallowed material into the
lungs. The larynx also moves upward and forward, which helps to open the esophagus for the passage of the swallowed material [9].
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O. Oğuz et al.
Respiration
During respiration, the rima glottidis, rima vestibuli, and vestibule are open. The
vocal folds may be further abducted during forced inspiration, by the action of the
posterior cricoarytenoid muscles, thus widening the rima glottidis and increasing
the diameter of the laryngeal airway [9].
Phonation
During phonation, the vocal cords and arytenoid cartilages are adducted. When air
is forced through the closed rima glottidis, the vocal cords vibrate against one
another to produce sounds [9].
3.2.2 Function andPhysiology oftheLarynx
The upper airway in adult humans traverses the digestive tract in the region of the
pharynx, complicating its sphincteric protection of the lower airway. By sharing a
common passageway with the upper digestive system, the larynx is also compromised in its respiratory performance by resultant ventilatory turbulence and, therefore, resistance. Thus, the anatomic conguration in adult humans that benets
phonatory purposes of the larynx simultaneously serves to compromise its sphincteric and respiratory functions. This functional dilemma is resolved at the laryngopharyngeal level by two important organic modications: structural adaptation and
delicate coordination among the three basic laryngeal functions as determined by
precisely organized brainstem reexes [10].
From a structural point of view, the protective function of the adult human larynx
is admittedly precarious by virtue of its low position in the neck. Other mammalian
species are provided with a relatively high-riding larynx, affording it a close approximation with structures of the posterior nasal cavities. The intranarial position of the
larynx, securing a continuous airway from the nose to the bronchi, therefore,
decreases the risk of pulmonary contamination by swallowed matter. This structural
modication is most obvious among certain cetaceans and herbivores but appears to
a lesser degree among carnivores that use an elongated epiglottis to affect nasolaryngeal connection during deglutition. In this regard, Negus considers the epiglottis to serve secondarily in an olfactory capacity, ensuring that inspired air enters
exclusively through the nose. By a series of anatomic demonstrations in macrosmatic animals, this contention appears very convincing and is supported by later
histologic work identifying epiglottic chemoreceptors similar in structure to taste
buds of the oral cavity, implying epiglottic participation in chemosensory perception as well [11].
In adult humans, the characteristic at, shield-like conguration of the epiglottis
serves to direct swallowed food laterally into the pyriform fossae, away from the
midline laryngeal aperture. Furthermore, in adult humans, the elevation of the larynx toward the nasal cavity during the height of deglutition exaggerates this protective function. Implicit in this maneuver is the role of the aryepiglottic folds, which
consist of mucous membrane, connective tissue, and muscle, extending from the
3 Structural andPhysiological Basis oftheUpper Respiratory Tract
45
epiglottic framework to the arytenoid bodies posteriorly. These lateral folds act as
ramparts to the larynx, allowing food to pass on either side of the epiglottis along
the gutter produced between each fold and the lateral pharyngeal wall. In this capacity, the cartilages of Santorini and Wrisberg, also called corniculate and cuneiform
cartilages, respectively, are contained in the aryepiglottic folds to provide added
support and stiffness to these ramparts of the laryngeal aperture. Therefore, from a
structural perspective alone, it would appear that the primary role of the supraglottic
larynx in adult humans lies in its protection of the lower airway [10].
In the human larynx the ability to perform as an effective valve depends on the
unique shelf-like conguration of its superior and inferior folds bilaterally represented. The ventricular folds or false cords, which are located superiorly, act as exit
valves, preventing the escape of air from the lower respiratory tract. When positioned by muscular contraction, they seal even more tightly as tracheal pressure is
increased from below. This feature of adducted false cords occurs independently of
muscle tone, a phenomenon attributable to their unique shape, which is characterized by the down-turned direction of their free margins. Such a conguration is
made possible by the lateral ventricles and is exaggerated by the superior extension
of the laryngeal saccules [10].
On the other hand, the true cords behaved as a one-way valve in the opposite
direction, obstructing the ingress of air. When approximated in the cadaver, the true
cords offered little resistance to pressure from below but resisted a pressure head
from above exceeding 140mmHg. Their ability to resist pressure from above was
not inuenced by closure of the false cords [10].
The false cords, therefore, prevent the egress of air from the lungs, and the true
cords with their up-turned margins are capable of impeding its ingress [10].
Therefore, it is not surprising that expectorative functions of the larynx remain
unimpaired in bilateral laryngeal paralysis. In this regard, passive closure of the
false cords alone appears essential to effective cough production. The valvular component of the true cords, on the other hand, is implicated in the clinical difculty
experienced in overcoming laryngeal spasms by abrupt pressure peaks of positive
pressure ventilation that only further serve to protectively seal the true cords.
Therefore, from a structural perspective, the false cords provide an expectorative
function, whereas the true cords assume a protective role in respiration [10].
Further structural modications in humans are relevant. The short arytenoid
vocal processes in humans effectively increase the relative length of the membranous true cords. Although obviously beneting the phonatory characteristic of the
larynx by maximizing its vibratory surface, these short vocal processes compromise
its respiratory capacity. In this regard, Negus calculates the optimum arytenoid
length to be 7/10 the length of the true cords, allowing a maximum cross-sectional
area at the glottis produced by the pivotal motion of the arytenoid bodies. Such an
optimum ratio of arytenoid to vocal cord length is found in the gazelle, with humans
possessing a 4:10 ratio instead [10].
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O. Oğuz et al.
3.2.2.1 Reflex Glottic Closure
Reex glottis closure is facilitated by (1) expiratory phase, (2) decreased arterial
partial pressure of carbon dioxide (pCO2), (3) increased arterial partial pressure of
oxygen (pO2), (4) negative intrathoracic pressure, and (5) hyperthermia. On the
other hand, reex glottic closure is inhibited by (1) inspiratory phase, (2) increased
arterial pCO2, (3) decreased arterial pO2, (4) positive intrathoracic pressure, and (5)
hypothermia [10].
In early inspiration, the mean threshold stimulus measured 0.37 V, 0.1 ms,
whereas in late inspiration, the mean threshold measured 0.36V, 0.1ms. In early
expiration, the mean threshold measured 0.28V, 0.1ms, whereas in late expiration,
the mean threshold measured 0.29V, 0.1ms. In the spontaneously breathing subject, therefore, the threshold of reex glottic closure seemed to increase on inspiration and decrease on expiration. In other words, reex glottic closure occurred more
readily in expiration than inspiration [10].
Effect ofCarbon Dioxide
The threshold of the glottic closure reex was determined with respect to precisely
controlled variations in arterial pCO2. The mean and range of three separate determinations were obtained in hypocapnia, normocapnia, and hypercapnia. For example, hypocapnia was produced by hyperventilating on room air, normocapnia by
administering room air during spontaneous respiration, and hypercapnia by administering 10% CO2 during spontaneous breathing. Arterial blood gas determinations
were conrmed in each test situation, such that arterial O2 tension (95 mmHg)
remained constant throughout this test period [10].
In the spontaneously breathing subject, iSLN stimuli were precisely phaselocked to early inspiration and early expiration to avoid variations caused by the
respiratory phase. During early inspiration, the mean threshold of the glottic closure
reex measured 0.21V at pCO2 of 25mmHg, 0.37V at pCO2 of 40mmHg, and
0.56V at pCO2 of 60mmHg. During early expiration, the threshold of the glottic
closure reex measured 0.21V at pCO2 of 25mmHg, 0.28V at pCO2 of 40mmHg,
and 0.40V at pCO2 of 60mmHg [10].
3.2.2.2 Neurophysiology ofRespiratory Function
Pertinent to respiratory laryngeal function is the role of the cricothyroid muscle,
known to be a vocal cord adductor and isotonic tensor. We have demonstrated that
this muscle contracts phasically with inspiration [12]. Although its inspiratory
adductor role would appear counterproductive to inspiration by narrowing the glottic aperture, its role in cord lengthening actually enhances the cross-sectional diameter of the glottis by increasing its anteroposterior dimension by 30%. Therefore, it
would appear that both posterior cricoarytenoid and cricothyroid muscles are driven
by the medullary respiratory center, the level of their activity regulated in eupneic
breathing by afferent impulses originating in the chest. Although posterior cricoarytenoid contraction increases the horizontal diameter of the glottic chink, its anteroposterior diameter is increased by phasic inspiratory contraction of the cricothyroid
muscle [10].
3 Structural andPhysiological Basis oftheUpper Respiratory Tract
47
In addition to its inspiratory function, cricothyroid expiratory activity is an
equally important consideration. In eupneic states, expiratory ow and duration are
principal determinants of respiratory frequency. As others have demonstrated in
both animal and human investigations, variations in respiratory rate result primarily
from changing the duration of the expiratory phase rather than the inspiratory phase
of the respiratory cycle [13, 14].
On a mechanical ventilator we observed the following interesting phenomenon.
Cricothyroid activity is evoked by positive intratracheal pressure, its contraction
synchronized with the phase of the ventilator. When the respiratory rate is mechanically increased from 20 to 40/min, cricothyroid activity appears to track synchronously with this rate change [10].
3.2.2.3 Neurophysiology ofPhonation
The phonatory function of the larynx is probably the least well understood of its
three basic functions. Because of advances in the investigative technique, many
established hypotheses based on animal models have been challenged, owing in
large measure to the advent of more sophisticated technology based on human study
[15–17]. High-speed cinematography, improved endoscopic techniques with the use
of the laryngeal stroboscope, and direct human EMG measurements made possible
by hooked wire electrodes are largely responsible for these newer additions [10].
It is generally agreed that speech results from the production of a fundamental
tone at the larynx and is modied by resonating chambers of the upper aerodigestive
tract. Intelligible speech, therefore, represents the combined effect of the larynx,
tongue, palate, and related structures of the oral vestibule. The production of the
fundamental tone is due to the vibration of the vocal folds against each other, generated by the passage of air between them. Vocal cord vibrations may be a passive
phenomenon representing the basis of the aerodynamic theory of sound generation.
Such a theory nds support in the observation that the completely paralyzed larynx
is capable of producing sound, as is the cadaver larynx when subglottic pressure is
forcefully increased. Obviously, phonation ceases when a tracheotomy is performed
for diversionary purposes [10].
The aerodynamic theory of sound production therefore replaces the neurochronaxic theory. The central generation of recurrent laryngeal nerve impulses produced
cord vibrations by active contraction of the thyroarytenoid muscles. Each vibration,
therefore, represented the result of beat-by-beat impulses through the recurrent
laryngeal nerve. This theory, no longer accepted, is of historical interest only [10].
Although sound production may be considered a passive function, the regulation
of its acoustic quality is not a passive phenomenon. Rather, vocal cord shaping and
positioning are under active neural regulation [18].
The cricothyroid (CT) muscle increases the fundamental frequency (F0) by tensing the vocal fold. The vocal fold is stretched, elongated, thinned, and slightly
adducted to the paramedian position as the vocal fold is lowered within the larynx.
These changes reduce the cross-sectional area of the vocal fold, reducing vibratory
mass and increasing F0. Vocalis muscle (Voc), on the other hand, generates the
opposite effect as it loosens and thickens the vocal fold. In addition, as it increases
48
O. Oğuz et al.
glottal resistance, it contributes to vocal intensity as subglottal pressure is increased.
Vocal control, therefore, is achieved by the coordinated efforts of respiratory, laryngeal, and articulatory muscles capable of producing great variations of tonal qualities characterizing the human voice [10].
References
1. Archer SM. Nasal physiology. In: Meyers AD, editor. Medscape. Updated 16 Nov 2021.
https://emedicine.medscape.com/article/874771- overview#a2. Accessed 21 Jun 2023.
2. Uzeloto JS, Ramos D, Silva BSA, etal. Mucociliary clearance of different respiratory conditions: a clinical study. Int Arch Otorhinolaryngol. 2021;25(1):e35–40.
3. Naclerio RM, Pinto J, Assanasen P, Baroody FM.Observations on the ability of the nose to
warm and humidify inspired air. Rhinology. 2007;45(2):102–11.
4. Chang EW.Nasal anatomy. In: Meyers AD, editor. Medscape. Updated 23 Jul 2015. https://
emedicine.medscape.com/article/835134- overview#a2. Accessed 21 Jun 2023.
5. Jafek BW.Anatomy and physiology of the nose. In: Jafek BW, Stark AK, editors. ENT secrets.
Philadelphia, PA: Hanley & Belfus; 1996. p.77–83.
6. Heidari Z, Mahmoudzadeh-Sagheb H, Khammar T, Khammar M.Anthropometric measurements of the external nose in 18-25-year-old Sistani and Baluch aborigine women in the southeast of Iran. Folia Morphol (Warsz). 2009;68(2):88–92.
7. Williams M, Eccles R.A model for the central control of airow patterns within the human
nasal cycle. J Laryngol Otol. 2016;130(1):82–8.
8. Kahana-Zweig R, Geva-Sagiv M, Weissbrod A, Secundo L, Soroker N, Sobel N.Measuring
and characterizing the human nasal cycle. PLoS One. 2016;11(10):e0162918.
9. Vashishta R. Larynx anatomy. In: Gest TR, editor. Medscape. Updated 7 Dec 2017. https://
emedicine.medscape.com/article/1949369- overview#a2. Accessed 21 Jun 2023.
10. Sasaki CT.Anatomy and development and physiology of the larynx. Part 1 Oral cavity, pharynx and esophagus. GI Motility online. 2006. https://doi.org/10.1038/gimo7. https://www.
nature.com/gimo/contents/pt1/full/gimo7.html. Accessed 21 Jun 2023.
11. Lalonde ER, Eglitis JA.Number and distribution of taste buds on the epiglottis, pharynx, larynx, soft palate, and uvula in human newborn. Anat Rec. 1961;140:91.
12. Suzuki M, Kirchner JA, Murakami Y. The cricothyroid as a respiratory muscle. Ann Otol
Rhinol Laryngol. 1970;79:1.
13. Bendixon HH, Smith GM, Mead J. Pattern of ventilation in young adults. J Appl Physiol.
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14. Remmers JE, Bartlett D Jr. Reex control of expiratory airow and duration. J Appl Physiol.
1977;42:80.
15. Stevens K, Hirano H.Vocal fold physiology. Tokyo: Tokyo University Press; 1981.
16. Bless DM, Abbs JH.Vocal fold physiology contemporary research and clinical issues. San
Diego: College Hill Press; 1983.
17. Baer T, Sasaki CT, Harris K.Laryngeal function in phonation and respiration. Boston: Little,
Brown; 1987.
18. Hirano M. Laryngeal muscles in singing. In: Hirano M, Kirchner JA, Bless D, editors.
Neurolaryngology: recent advances. Boston: Little, Brown; 1987.
Congenital Anomalies oftheUpper
Respiratory Tract
EmineKörkuyuYardımcı, CemalCingi,
EmmanuelP.Prokopakis, andNurayBayar Muluk
4.1 Introduction
Infants and young children often experience morphological and functional obstruction due to congenital anomalies of the upper airway, which includes the nasal oropharynx and extends to the subglottis. As a result, they may have trouble breathing.
This section will examine the most frequent upper airway congenital anomalies
according to their primary anatomic location [1]. In children younger than 2½ years
old, anomalies of the larynx account for 85% of cases of stridor. It is vital to distinguish between self-limiting and terminal conditions while working with these
patients [2].
4
E. K. Yardımcı
Department of Otolaryngology, Head and Neck Surgery, Adana Çukurova Public Hospital,
Adana, Turkey
C. Cingi
Department of Otorhinolaryngology, Medical Faculty, Eskisehir Osmangazi University,
Eskisehir, Turkey
e-mail: cemal@ogu.edu.tr
E. P. Prokopakis
Department of Otorhinolaryngology, University of Crete, School of Medicine, Crete, Greece
N. Bayar Muluk (*)
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, 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_4
49
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E. K. Yardımcı et al.
4.2 Congenital Anomalies oftheNose andNasopharynx
Newborns must breathe through their noses, so any blockage there could be dangerous. Some possible causes include choanal atresia, a narrowed pyriform aperture,
and even malignant tumors, including glioma, encephalocele, dermoid, and
teratoma.
4.2.1 Choanal Atresia
In congenital choanal atresia, bone or soft tissue at birth blocks the nasal cavity’s
posterior choanae. The congenital nasal airway defect known as choanal atresia
(CA) is associated with various symptoms, from complete airway obstruction to
chronic sinusitis. Roederer rst recognized this medical condition in 1755 [3]; later,
in 1829, Oto etal. provided additional information about the deformity of the palatine bones. Only one in every 5000–7000 babies is diagnosed with choanal atresia
[4]. In 1910, researchers found that bony atresia accounted for 90% of deformity
cases, while membrane atresia accounted for 10%. One research of 63 patients
found that 29% had pure bone atresia, 71% had mixed membranous and bone atresia, and no pure membranous atresia was detected [5] based on CT scans and histologic investigation (Fig.4.1).
The clinical appearance of CA can range from acute airway obstruction to
chronic recurrent sinusitis, with the latter being more common in patients with
CHARGE syndrome and craniofacial deformities.
This problem should be diagnosed soon after delivery. A 6 or 8 Fr suction catheter is inserted via the nostrils, methylene blue dye is tested, cotton swabs are used,
and a laryngeal mirror is used for the initial clinical evaluation. Understanding the
cause of nasal blockage by measuring the amount of resistance experienced is possible. A deviation of the nasal septum or inferior turbinate is likely to cause an
obstruction 1–2cm from the ala rim in neonates, while an obstruction 3–3.5 cm
Fig. 4.1 Endoscopic view of the atretic plate of the choanal atresia
4 Congenital Anomalies oftheUpper Respiratory Tract
51
from the alar rim indicates the level posterior choanae [6]. After the infant has been
appropriately prepared, including nasal decongestion and mucus suctioning, the
diagnosis of choanal atresia can be conrmed via examination with a exible nasal
endoscope. A CT scan is recommended for diagnosing choanal atresia because it
can more clearly dene the anatomy of the atretic area, such as the thickness of the
atretic plate and the existence and thickness of a bony plate. CT helps distinguish
choanal atresia from other causes of nasal obstruction and elucidates the condition’s
nature and severity. Pyriform aperture stenosis, nasolacrimal duct cysts, enlarged
turbinates, septal dislocation and deviation, antrochoanal polyp, and nasal neoplasm
[7] are all potential causes.
Choanal atresia is treated with a surgical procedure. The goals are to restore choanal
patency while minimizing invasiveness, preventing recurrences, and interfering with
the patient’s natural craniofacial growth. Surgery for unilateral choanal atresia can be
delayed until school age when the area’s anatomy is more similar to that of adults and
is, therefore, less urgent. However, it must be observed for signs of a breathing disorder.
The saline nasal spray is another option for maintaining a clear nasal passage. When
available, a McGovern nipple, an intraoral nipple with a large opening created by cutting off its end and securing it in the mouth with ties around the infant’s occiput, is used
to maintain an adequate oral airway until the atresia plate can be perforated and the
infant can breathe normally. The proposed surgical routes are transpalatal, transeptal,
sublabial, transanal, and transnasal. Before the emergence of the endoscopic endonasal
method in recent decades, the transpalatal procedure was the norm. Since the endoscopic endonasal technique for the repair of choanal atresia is effective with fewer
surgical complications than traditional procedures [6, 7], many surgeons are increasingly turning to it. Comparison and meaningful interpretation of various studies are
difcult, if not impossible, due to differences in surgical techniques, duration of stenting, or use of adjunct therapy (e.g., mitomycin), and the lack of standardized outcome
measures (i.e., a denition for choanal patency and surgical failure) [6].
4.2.2 Pyriform Aperture Stenosis
Rare and potentially fatal neonatal nasal obstruction [8] is caused by congenital
nasal pyriform stenosis (CNPS). The pyriform aperture is the frontmost and smallest of the nasal airway openings made of bone. Laterally, it is bounded by the maxillary nasal process; inferiorly, by the horizontal process of the maxilla and the
anterior nasal spine; and superiorly, by the nasal bones themselves (position 9). CT
scans can accurately diagnose pyriform aperture stenosis by acquiring thin
(1.5–3.0mm), continuous axial sections in a plane parallel to the anterior hard palate. Showing the narrowing on consecutive sections is crucial because oblique
imaging can produce a false impression of narrowing [9]. In infants aged 0–6months,
the pyriform sinus should measure between 8.8 and 17.2 mm (median
width=13.5mm). If a term child has a pyriform aperture width of less than 3mm
on one side or the combined width of both pyriform apertures is less than 8mm,
then the diagnosis is CNPS [10].