Pediatric Airway Surgery
Editor(s): Hartnick, C.J. (Boston, MA)
Hansen, M.C. (Boston, MA)
Gallagher, T.Q. (Portsmouth, VA)
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Introduction
Laryngeal Development and Anatomy
Kakodkar K.A.a · Schroeder, Jr. J.W.b,c · Holinger L.D.b,c
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Hartnick CJ, Hansen MC, Gallagher TQ (eds): Pediatric Airway Surgery. Adv Otorhinolaryngol. Basel, Karger, 2012, vol 73, pp 1–11
https://doi-org.ezp-prod1.hul.harvard.edu/10.1159/000334108
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Abstract
Knowledge of laryngeal and tracheobronchial development and anatomy is essential to the pediatric airway endoscopist. Normal and pathologic airway anatomy is discussed in this chapter.
© 2012 S. Karger AG, Basel
The Larynx
Certain aspects of laryngeal development and anatomy deserve particular mention. Emphasis is placed upon the infant larynx and congenital laryngeal stenosis.
Laryngeal Development
Human development is divided into the embryonic period (the first 8 weeks of gestation) and the subsequent fetal period (the last 32 weeks of gestation) [1]. The Carnegie Staging System assigns 23 stages to the embryonic period. Each stage has a characteristic feature not seen in a previous stage. Laryngeal development is first seen in stage 11 and proceeds to stage 23 and can be divided into eight phases (fig. 1).
In phase I (Carnegie stage ll), the first sign of the respiratory system is seen as an epithelial thickening along the ventral aspect of the foregut known as the respiratory primordium. In this stage, the foregut lumen is widely patent.
In phase II (Carnegie stage 12), a ventral outpouching termed the respiratory diverticulum (RD) of the foregut lumen called the primitive pharyngeal floor expands into the respiratory primordium. The primitive pharyngeal floor eventually develops in the glottic region of the adult larynx. The cephalic portion of the RD eventually develops into the infraglottic region. The RD gives rise to bilateral projections called bronchopulmonary buds that eventually develop into the lower respiratory tract.
In phase III (Carnegie stages 13 and 14), the upper foregut region and the RD migrate superiorly and the bronchopulmonary buds are drawn caudally and inferiorly [2]. As a result, the two main bronchi and carina develop. As the distance between the RD and the carina lengthens, the trachea forms. During this phase, as the trachea and esophagus lengthen, vascular compromise may cause esophageal atresia (EA), tracheoesophageal fistula (TEF), tracheal agenesis or tracheal stenosis with complete rings.
In phase IV (Carnegie stage 15), the ventral portion of the primitive laryngopharynx becomes compressed bilaterally by the developing mesoderm of the laryngeal cartilages, muscles, and the four branchial arch arteries. Eventually, the obliteration and the ventral lumen of the primitive laryngopharynx give rise to the epithelial lamina.
Fig. 1.
Eight phases of laryngeal development.
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In phase V (Carnegie stage 16), the epithelial lamina continues to obliterate the primitive laryngopharynx in a ventral to dorsal direction leaving a narrow communication between the hypopharynx and the infraglottis. A depression called the laryngeal cecum begins to develop between the arytenoid swellings and epiglottis. The laryngeal cecum descends along the ventral aspect of the epithelial lamina giving the T-shaped entrance to the primitive laryngopharynx more definition.
In phase VI (Carnegie stages 17 and 18), the laryngeal cecum continues its caudal descent until it reaches the glottic region. In phase VII (Carnegie stages 19 and 23), the epithelial lamina begins to recanalize from a dorsocephalic to ventrocaudal direction. The last portion of the primitive laryngopharynx to recanalize is at the glottic level. Incomplete recanalization of the epithelial lamina can result in supraglottic and glottic webs and atresia. These atresias can be divided into three types. Type I consists of a supraglottic obstruction, absent vestibule and stenosis subglottis. Type 2 is a supraglottic obstruction that separates the primitive vestibule from the normal subglottis. In type 3, a perforated membrane partly obstructs the glottis [3].
Phase VIII of laryngeal development corresponds to the fetal period. The Carnegie staging system concludes at the end of the embryogenic period and does not apply to the fetal period. Ventral outgrowths from the lateral aspects of the laryngeal cecum give rise to the laryngeal ventricles. With complete recanalization of the epithelial lamina, a complete communication is established between the supraglottis and infraglottis.
In the fetal period, the larynx grows, becomes more defined and develops neurologic reflexes. Myenteric plexuses and ganglion cells are differentiated by 13 weeks of gestation. Fetuses begin swallowing amniotic fluid by 16 weeks’ gestation. The cartilaginous vocal processes of the arytenoids as well as the ventricle and saccule are defined by this stage. Fibroelastic cartilage appears in the epiglottis in the 5th and 6th months. The corniculate cartilages develop at this time as well. During the second trimester, fetal breathing and laryngeal movement and coordination are apparent.
Laryngeal Anatomy
Cuneiform Cartilages
The cuneiform cartilages are two elastic cartilages variable in size, resting within the aryepiglottic folds anterosuperior to the arytenoid and corniculate cartilages, and without any direct articulation with the arytenoid cartilages [4] (fig. 2).
Cricoid Cartilage
The cephalad half of the cricoid cartilage is V shaped; in contrast, the caudad portion of the cricoid ring is a smooth, round circle (fig. 2). This produces an elliptical shape to the upper subglottic laryngeal lumen, which is somewhat more apparent in the infant than the adult.
Fig. 2.
The infant larynx. The saccule projects superiorly from the anterior roof of the ventricle. The hyoid bone is anterior to the thyroid notch.
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Posterior Glottis
The anatomic boundaries defining the posterior glottis are the posterior wall of the glottis, the lateral walls of the posterior glottis, and the cartilaginous portion of the vocal folds [5]. The anterior limit of the posterior glottis is defined by the tip of the vocal process of the arytenoids.
During vocal adduction, the posterior part of the larynx closes completely, not at the glottis but at the supraglottis, resulting in the formation of a conical space in the posterior glottis that can be viewed only from below [5]. Therefore, the posterior glottis is not a commissure. The posterior glottis functions primarily for respiration and the anterior glottis for phonation.
Laryngeal Ventricle and Saccule
The laryngeal ventricle is a fusiform fossa bounded below and above the true and false vocal cords. The anterior part of the roof of the ventricle leads up into a blind pouch of mucous membrane called the saccule. The laryngeal saccule rises vertically between the false vocal cord and the inner surface of the thyroid cartilage [6].
The Infant Larynx
The infant larynx differs from the adult larynx in several aspects. An accurate understanding of the anatomy and histopathology of the larynx is essential in treating causes of airway obstruction, such as congenital laryngeal stenosis, as well as incomplete development resulting in posterior laryngeal cleft.
Location
The infant larynx differs from the adult larynx in a few key aspects. In the infant larynx, the inferior margin of the cricoid cartilage is at the level of the fourth cervical vertebra (C4) and the tip of the epiglottis is at C1. The thyroid cartilage is within the arch of the hyoid bone and slightly inferior to it (fig. 2). This laryngeal positioning allows for the epiglottis to rest posterior to the soft palate, which permits simultaneous sucking and respiration contributing to the obligate nasal breathing of the newborn [7]. As one progresses through childhood, the cricoid cartilage descends to the level of C6 and then to the level of C7 in the adult.
Size
At birth, the infant larynx is approximately one third the size of the adult larynx. Several structures are relatively larger in the infant larynx (see fig. 4). The vocal processes of the arytenoids comprise slightly more than half the infant glottis, whereas in the adult, they comprise approximately one seventh to one fourth the length of the glottis [5]. The cuneiform cartilages, arytenoids, and soft tissue that comprise the posterior supraglottic larynx are larger in the infant. At endoscopy, the infant larynx appears anteriorly displaced, the arytenoids are prominent and the membranous portion of the vocal fields is short. At the level of the glottis, the vocal folds are 6-8 mm in length. The posterior glottis is approximately 3-4 mm in width. The subglottic larynx has a diameter of 5-7 mm; a diameter of 4 mm represents a subglottic stenosis [8]. A 3.5-mm endotracheal tube or a size 3 bronchoscope (5 mm outside diameter) should pass through the larynx of a newborn infant without substantial resistance. The superior margin of the first tracheal arch forms a ridge often prevalent at endoscopy.
Fig. 3.
Normal larynx of a 3-year-old boy. Tubular omegashaped epiglottis is noted.
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Configuration
The infant epiglottis is more narrow, posterior, and tubular or omega shaped when compared to the adult epiglottis (fig. 3). The lumen at the glottis is somewhat pentagonal in shape during inspiration. As the vocal folds taper inferiorly into the subglottic larynx, the lumen is elliptical, with the greater diameter in the anteroposterior dimension. At the inferior aspect of the cricoid cartilage, the lumen is round (fig. 4). When viewed in the coronal plane, the lumen is narrower at the top and wider at the bottom, resembling an inverted funnel. However, when viewed in the sagittal plane, the laryngeal lumen is slightly larger superiorly at the glottic level and narrower at the inferior aspect of the cricoid cartilage. Congenital cricoid abnormalities are commonly encountered and discussed in the section below titled ‘Congenital Laryngeal Stenosis’ [6].
Fig. 4.
Horizontal sections through the larynx of an 18-month-old child corresponding to the superior most section of the larynx at the apex of the epiglottis to the inferior most section at the inferior aspect of the cricoid cartilage (a-h, respectively). a Omega-shaped epiglottis. b Hyoid bone located anterior to the thyroid cartilage. c Saccule extends superiorly to this level. d Hyoid again noted to be anterior to the thyroid notch. e Saccule located between the false vocal fold and the inner lamina of the thyroid cartilage. f Superior section with V-shaped posterior cricoid cartilage. g Mid-section through cricoid cartilage with posterior V shape. h Inferior section through cricoid cartilage with a round shape. From Holinger L and others: Pediatric Laryngology and Bronchoesophagology, Lippincott-Raven, 1997.
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Tissue Consistency
Cartilage, muscle, and submucosal tissue are softer and more pliable in the infant larynx. Looser, less fibrous, submucosal tissue permits passive movement with respiration, and greater reaction and swelling with a more significant loss of lumen in inflammatory conditions [6].
Congenital Laryngeal Stenosis
Subglottic stenosis is one of the most common causes of airway obstruction. It can be categorized as either acquired or congenital, by clinical or anatomic characteristics, as well as by histopathology Acquired subglottic stenosis is narrowing of the subglottic airway secondary to a traumatic or inflammatory event, most commonly endotracheal tube intubation usually in association with laryngopharyngeal reflux and infection. Subglottic stenosis is considered congenital when there is no known cause of the narrowing. Congenital subglottic stenosis, the third most common congenital laryngeal anomaly following laryngomalacia and vocal fold paralysis, is highlighted in this section [6].
With regards to the histopathologic classification, subglottic stenosis can be further categorized as either cartilaginous or soft tissue in nature. Cartilaginous subglottic stenosis can involve either a cricoid cartilage deformity or a trapped first tracheal ring. The elliptic cricoid is the most frequently diagnosed abnormal shape resulting in congenital subglottic stenosis. The ellipse pattern is due to a transverse diameter that is shorter than the anterioposterior diameter, resulting in less than normal cross-sectional area. These measurements are equal in the normal larynx. The cricoid cartilage can also assume a flattened shape with a transverse diameter greater than the anterioposterior diameter. The flattened cricoid can be associated with a trapped first tracheal ring, which involves the first tracheal ring telescoping within the cricoid cartilage causing the airway to be narrowed [9].
Upon clinical evaluation, symptoms can vary from mild stridor to severe obstruction due to the extent of the stenosis. Patients with severe obstruction may have apneic episodes, suprasternal and subcostal retractions, dyspnea, and cyanosis. Patients with congenital subglottic stenosis, particularly younger than 6 months, can also present with recurrent or persistent croup. In such patients, the underlying congenital pathology may be exacerbated by reflux events or infection, and congenital stenosis must be considered.
Evaluation of congenital laryngeal stenosis in addition to a thorough history and physical examination includes flexible fiber-optic laryngoscopy and imaging. Direct laryngoscopy and rigid bronchoscopy are vital in the assessment of congenital stenosis and also allow examination for possible synchronous airway lesions. Treatment is individualized and depends upon the nature and severity of the stenosis as well as the patient's physical condition. In general, congenital subglottic stenosis causing 50% or greater airway obstruction (Meyer-Cotton grade II or greater) may require surgical intervention, which can either be external or endoscopic approaches to cricoid expansion described in greater detail in subsequent chapters with emphasis upon surgical technique [9].
Posterior Laryngeal Cleft
The congenital posterior laryngeal cleft is a rare condition and is characterized by the incomplete development of the tracheoesophageal septum. The incidence of laryngeal cleft is approximately 1 in 10,000-20,000 live births and is more common in boys than girls, with a ratio of 5:3 [10]. A higher incidence of laryngeal cleft is reported with Pallister-Hall and Opitz-Frias syndromes [11].
Stridor, choking, cyanosis, and signs of aspiration are typical manifestations in newborns with congenital posterior laryngeal clefts. The stridor is often inspiratory but can be expiratory when associated with tracheomalacia. Other conditions that should be kept in mind when considering posterior laryngeal cleft include esophageal stricture, TEF, cricopharyngeal spasm, laryngomalacia, gastroesophageal reflux, and vocal fold paralysis.
The diagnosis of laryngeal clefts includes a high index of suspicion along with a thorough history and physical examination. Microlaryngoscopy under general anesthesia remains the gold standard in diagnosing posterior laryngeal clefts. Palpation with a probe is essential to determine the type of laryngeal cleft. In 1989, Benjamin and Inglis [10] presented a classification system in which 4 types of clefts were described: type 1 is a supraglottic interarytenoid defect that extends inferiorly no further than the level of the true vocal folds; in type 2, the cricoid lamina is partially involved with extension of the cleft below the level of the true vocal folds; type 3 is a total cricoid cleft extending inferiorly with or without further extension in the cervical trachea; type 4 extends into the posterior wall of the thoracic trachea [11].
Treatment of posterior laryngeal clefts involves initial stabilization of the infant’s airway. The timing and approach for surgical repair depends on the severity of symptoms and the type of cleft present. Small clefts may be missed that often do not require surgical intervention. More significant clefts extending below the vocal folds are typically addressed via a cervical approach [6].
The Trachea and Bronchi
The anatomy of the normal tracheobronchial tree is presented in this section.
Trachea
The trachea extends from the inferior margin of the cricoid cartilage to the carina. The inferior end of the trachea is at the level of the fifth thoracic vertebra or the sternal angle. The trachea is 4 cm long in a full-term newborn infant and 11-13 cm long in an adult. The diameter of the trachea is 4-5 mm in a full-term newborn and 12-23 mm in an adult. The posterior or membranous portion of the trachea, or pars membranosa, is composed of the trachealis muscle and elastic and fibrous tissue. The ratio of cartilaginous to membranous trachea normally is 4.5:1. Variations in the tracheal cross-section diameter occur during breathing and coughing as a result of changes in head and neck position as well as intrathoracic pressure [12].
Bronchi
The trachea bifurcates at the carina, which is relatively acute in adults but less so in infants. The right main bronchus branches off at a 25° angle from the trachea, the left at a 45° [13]. Horseshoeshaped cartilages support the main bronchi. The right main bronchus is shorter but larger in diameter than the left. The right main bronchus is straight, whereas the left often has a gentle curvature.
In normal humans, there are three lobar bronchi on the right and two on the left. Usually, there are ten segmental bronchi on the right and eight on the left. The lobar bronchi most often are constant, but there is considerable variability in the segmental bronchi. Cartilage plates support the lobar, segmental, and smaller distal bronchi [14].
The right main bronchus branches into the upper lobe bronchus and the bronchus intermedius. The upper lobe bronchus divides into anterior, posterior, and apical segments. The bronchus intermedius divides into the middle lobe and lower lobe bronchi. The middle lobe bronchus divides into medial and lateral segments. The first branch of the lower lobe bronchus is the superior segment. The remainder of the lower lobe divides into medial, anterior, lateral and posterior basal segments.
The left main bronchus divides into upper and lower lobes. The upper lobe bronchus then divides into the upper division and the lingual. The upper division has anterior and apicoposterior segments. The lingual has superior and inferior segments. The first branch of the lower lobe is the superior segment. The three basilar segments of the left lower lobe are the anteromedial, lateral, and posterior basal segments [6].
Adjacent Vascular and Cardiac Anomalies
Knowledge of adjacent anatomy and vasculature becomes particularly important when assessing etiology of external compression of the tracheobronchial tree. Tracheomalacia is the abnormal narrowing of the tracheal walls, and is classified as primary or secondary. In primary tracheomalacia, the defect is intrinsic to the trachea. No extrinsic factors cause compression or distortion, and the cartilage-to-membranous trachea ratio may be 3 to 1, or even 2 to 1. The flattened posterior membranous trachea collapses forward during expiration (and more so with coughing), often touching the anterior wall. In secondary tracheomalacia, other factors are related to the pathology. Similarly, bronchomalacia is the abnormal narrowing of the bronchial walls, which can also be secondary to adjacent pathology. In particular, certain types of vascular and cardiac abnormalities are noted to cause specific presenting symptoms and characteristic endoscopic findings and are discussed below.
Fig. 5.
Endoscopic depiction of the tracheobronchial tree and typical findings secondary to adjacent vascular pathology and cardiovascular disease.
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Aberrant Innominate Artery
An aberrant innominate artery may cause compression of the trachea seen on endoscopy as compression of the right anterolateral wall of the upper trachea, giving the lumen a triangular shape (fig. 5). Lifting the tip of the bronchoscope against the pulsatile artery diminishes the right brachial pulse. This compression can lead to a variety of presenting symptoms, including a croupy or barky cough, wheezing, expiratory stridor, or apneic episodes. The differential diagnosis to be considered includes central apnea, gastroesophageal reflux with apnea, and other causes of apparent life-threatening events [6].
Patients with severe obstruction and subsequent life-threatening episodes, recurrent pneumonia due to ineffective clearance of secretions, and progressive obstruction may warrant suspension of the innominate artery and aorta to the posterior surface of the sternum (innominate arteriopexy). Yet, the majority of patients with an aberrant innominate artery resulting in extrinsic airway compression do not require surgical intervention due to its self-limiting nature.
Double Aortic Arch
The double aortic arch is a relatively rare congenital anomaly in which two aortic arches form a complete vascular ring that encircles the trachea and esophagus, forming a complete ring (fig. 5). Most commonly, there is a dominant right arch posterior and a hypoplastic left arch anterior to the trachea and esophagus. The two arches subsequently join the descending aorta, which is usually on the left side.
Symptoms related to this anomaly are due to the compression of the trachea and/or the esophagus and usually begin at birth. Diagnosis can often be suspected or made by radiograph, barium esophagram, or echocardiography. Computer tomography or magnetic resonance imaging are more specific and note the anatomic relationship of the aortic arches to the trachea and esophagus. This aids the cardiovascular surgeon in planning surgical division of the ring. Many patients experience almost immediate postoperative resolution of obstructive symptoms, whereas in some it takes 1-2 years for respiratory symptoms to improve [6].
Pulmonary Artery Sling
The pulmonary artery (PA) sling is associated with an absent left PA and is, instead, associated with an aberrant left PA arising from the right PA. Upon endoscopy, this vascular anomaly may cause compression of the right main bronchus, which may have a slit-like lumen and subsequently courses between the trachea and esophagus (fig. 5). The lower trachea is narrowed from the right side. Treatment includes surgery to divide and reimplant the artery, improving obstructive symptoms [15].
Congenital Cardiac Defects
Pulmonary hypertension secondary to a left-to-right shunt can lead to enlargement of the pulmonary arteries and subsequent compression of the left main bronchus (fig. 5). The left main bronchus normally traverses the superior aspect of the left atrium and left pulmonary veins, also passing adjacent to the pulmonary arteries. Patients with ventral septal defects or patent ductus arteriosus may have such compression secondary to left-to-right shunt and resulting pulmonary hypertension [15].
Symptoms depend upon the severity of airway obstruction and may include wheezing, recurrent pneumonia, atelectasis, or lobar emphysema. Severe cases may include ventilator dependence due to high mean airway pressures needed to overcome compressed airways. Bronchoscopy may yield left-sided bronchial compression. Computed tomography of the chest with contrast, magnetic resonance imaging, or cardiac catheterization may reveal the underlying pathology. Treatment is targeted towards relief of pulmonary hypertension and subsequent airway compression. PA plication or arteriopexy are rarely indicated [16].
Tracheoesophageal Fistula and Esophageal Atresia
A TEF is an abnormal connection between the esophagus and the trachea. Congenital EA results in two blind-ended pouches, an upper and a lower, which may or may not communicate with the tracheobronchial tree resulting in a TEF. Presenting symptoms include feeding and/or respiratory difficulties as well as persistent aspiration. TEF and EA occur in approximately 1 in 3,000-5,000 births. The five forms of EA and TEF are illustrated in figure 6. Treatment is surgical and involves primary extrapleural repair of EA with division and oversewing of the distal fistula. Postsurgical complications include tracheomalacia, esophageal stricture, recurrent fistula, and gastroesophageal reflux. The prognosis of surgical intervention is good, but respiratory complications may be severe [17].
Fig. 6.
Five types of EA and tracheoesophageal atresia. Type C is the most common.
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Conclusions
The pediatric airway endoscopist must be well versed in the normal and pathologic anatomic and developmental variations. Knowledge of key structural features involving the larynx, trachea and bronchi is essential in understanding the diagnosis and treatment of congenital laryngeal stenosis, posterior laryngeal cleft, external compression secondary to adjacent vascular and cardiac anomalies, as well as EA and TEF.
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References
Henick DH: Three dimensional analysis of murine laryngeal development. Ann Otol Rhinol Laryngol Suppl 1993;159:3-24
O'Rahilly R, Müller F: Chevalier Jackson lecture. Respiratory and alimentary relations in staged human embryos. New embryological data and congenital anomalies. Ann Otol Rhinol Laryngol 1984;93:421-429
Zaw-Tun HI: Development of congenital laryngeal atresias and cleft. Ann Otol Rhinol Laryngol 1988;97:353
Bosma JF: Anatomy of the Infant Head. Baltimore, The John Hopkins University Press 1985;
Hirano M, Kurita S, Kiyokawa K, Sato K: Posterior glottis. Morphological study in excised human larynges. Ann Otol Rhino Laryngol 1986;95:576-581
Holinger LD: Pediatric Laryngology & Bronchoesophagology. Philadelphia, Lippincott Raven 1997;
Holinger PH, Johnson KC, Schiller F: Congenital anomalies of the larynx. Ann Otol Rhino Laryngol 1954;63:581-606
Schild JA: Relationship of laryngeal dimensions to body size and gestational age in premature, neonates and small infants. Laryngoscope 1984;94:1284-1292
Schroeder JW, Holinger LD: Congenital laryngeal stenosis. Otol Clin North Am 2008;41:865-875
Benjamin B, Inglis A: Minor congenital laryngeal clefts: diagnosis and classification. Ann Otol Rhinol Laryngol 1989;98:417-420
William PL, Warwick R: Gray’s Anatomy ed 36Philadelphia, WB Saunders, 1980;1246
Hollinshead WH, Rosse C: Textbook of Anatomy ed 4Philadelphia, Harper & Row, 1985;494
(eds) Williams PL, Warwick R: Gray’s Anatomy ed 36Philadelphia, WB Saunders, 1980;1257
Landing BH, Dixon LG: Congenital malformations and genetic disorders of the respiratory tract. Am Rev Respir Dis 1979;120:151-185
Holinger PH: Congenital anomalies of the tracheobronchial tree. Postgrad Med 1964;26:454-462
Benjamin B, Pham T: Diagnosis of H-type tracheoesophageal fistula. J Pediatr Surg 1991;26:667-671
Benjamin B: Endoscopy in esophageal atresia and tracheoesophageal fistula. Ann Otol Rhinol Laryngol 1981;90:376
Editor(s): Hartnick, C.J. (Boston, MA)
Hansen, M.C. (Boston, MA)
Gallagher, T.Q. (Portsmouth, VA)
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Introduction
Laryngeal Development and Anatomy
Kakodkar K.A.a · Schroeder, Jr. J.W.b,c · Holinger L.D.b,c
Author affiliations
Corresponding Author
Hartnick CJ, Hansen MC, Gallagher TQ (eds): Pediatric Airway Surgery. Adv Otorhinolaryngol. Basel, Karger, 2012, vol 73, pp 1–11
https://doi-org.ezp-prod1.hul.harvard.edu/10.1159/000334108
Abstract
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Extras : 6
Abstract
Knowledge of laryngeal and tracheobronchial development and anatomy is essential to the pediatric airway endoscopist. Normal and pathologic airway anatomy is discussed in this chapter.
© 2012 S. Karger AG, Basel
The Larynx
Certain aspects of laryngeal development and anatomy deserve particular mention. Emphasis is placed upon the infant larynx and congenital laryngeal stenosis.
Laryngeal Development
Human development is divided into the embryonic period (the first 8 weeks of gestation) and the subsequent fetal period (the last 32 weeks of gestation) [1]. The Carnegie Staging System assigns 23 stages to the embryonic period. Each stage has a characteristic feature not seen in a previous stage. Laryngeal development is first seen in stage 11 and proceeds to stage 23 and can be divided into eight phases (fig. 1).
In phase I (Carnegie stage ll), the first sign of the respiratory system is seen as an epithelial thickening along the ventral aspect of the foregut known as the respiratory primordium. In this stage, the foregut lumen is widely patent.
In phase II (Carnegie stage 12), a ventral outpouching termed the respiratory diverticulum (RD) of the foregut lumen called the primitive pharyngeal floor expands into the respiratory primordium. The primitive pharyngeal floor eventually develops in the glottic region of the adult larynx. The cephalic portion of the RD eventually develops into the infraglottic region. The RD gives rise to bilateral projections called bronchopulmonary buds that eventually develop into the lower respiratory tract.
In phase III (Carnegie stages 13 and 14), the upper foregut region and the RD migrate superiorly and the bronchopulmonary buds are drawn caudally and inferiorly [2]. As a result, the two main bronchi and carina develop. As the distance between the RD and the carina lengthens, the trachea forms. During this phase, as the trachea and esophagus lengthen, vascular compromise may cause esophageal atresia (EA), tracheoesophageal fistula (TEF), tracheal agenesis or tracheal stenosis with complete rings.
In phase IV (Carnegie stage 15), the ventral portion of the primitive laryngopharynx becomes compressed bilaterally by the developing mesoderm of the laryngeal cartilages, muscles, and the four branchial arch arteries. Eventually, the obliteration and the ventral lumen of the primitive laryngopharynx give rise to the epithelial lamina.
Fig. 1.
Eight phases of laryngeal development.
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In phase V (Carnegie stage 16), the epithelial lamina continues to obliterate the primitive laryngopharynx in a ventral to dorsal direction leaving a narrow communication between the hypopharynx and the infraglottis. A depression called the laryngeal cecum begins to develop between the arytenoid swellings and epiglottis. The laryngeal cecum descends along the ventral aspect of the epithelial lamina giving the T-shaped entrance to the primitive laryngopharynx more definition.
In phase VI (Carnegie stages 17 and 18), the laryngeal cecum continues its caudal descent until it reaches the glottic region. In phase VII (Carnegie stages 19 and 23), the epithelial lamina begins to recanalize from a dorsocephalic to ventrocaudal direction. The last portion of the primitive laryngopharynx to recanalize is at the glottic level. Incomplete recanalization of the epithelial lamina can result in supraglottic and glottic webs and atresia. These atresias can be divided into three types. Type I consists of a supraglottic obstruction, absent vestibule and stenosis subglottis. Type 2 is a supraglottic obstruction that separates the primitive vestibule from the normal subglottis. In type 3, a perforated membrane partly obstructs the glottis [3].
Phase VIII of laryngeal development corresponds to the fetal period. The Carnegie staging system concludes at the end of the embryogenic period and does not apply to the fetal period. Ventral outgrowths from the lateral aspects of the laryngeal cecum give rise to the laryngeal ventricles. With complete recanalization of the epithelial lamina, a complete communication is established between the supraglottis and infraglottis.
In the fetal period, the larynx grows, becomes more defined and develops neurologic reflexes. Myenteric plexuses and ganglion cells are differentiated by 13 weeks of gestation. Fetuses begin swallowing amniotic fluid by 16 weeks’ gestation. The cartilaginous vocal processes of the arytenoids as well as the ventricle and saccule are defined by this stage. Fibroelastic cartilage appears in the epiglottis in the 5th and 6th months. The corniculate cartilages develop at this time as well. During the second trimester, fetal breathing and laryngeal movement and coordination are apparent.
Laryngeal Anatomy
Cuneiform Cartilages
The cuneiform cartilages are two elastic cartilages variable in size, resting within the aryepiglottic folds anterosuperior to the arytenoid and corniculate cartilages, and without any direct articulation with the arytenoid cartilages [4] (fig. 2).
Cricoid Cartilage
The cephalad half of the cricoid cartilage is V shaped; in contrast, the caudad portion of the cricoid ring is a smooth, round circle (fig. 2). This produces an elliptical shape to the upper subglottic laryngeal lumen, which is somewhat more apparent in the infant than the adult.
Fig. 2.
The infant larynx. The saccule projects superiorly from the anterior roof of the ventricle. The hyoid bone is anterior to the thyroid notch.
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Posterior Glottis
The anatomic boundaries defining the posterior glottis are the posterior wall of the glottis, the lateral walls of the posterior glottis, and the cartilaginous portion of the vocal folds [5]. The anterior limit of the posterior glottis is defined by the tip of the vocal process of the arytenoids.
During vocal adduction, the posterior part of the larynx closes completely, not at the glottis but at the supraglottis, resulting in the formation of a conical space in the posterior glottis that can be viewed only from below [5]. Therefore, the posterior glottis is not a commissure. The posterior glottis functions primarily for respiration and the anterior glottis for phonation.
Laryngeal Ventricle and Saccule
The laryngeal ventricle is a fusiform fossa bounded below and above the true and false vocal cords. The anterior part of the roof of the ventricle leads up into a blind pouch of mucous membrane called the saccule. The laryngeal saccule rises vertically between the false vocal cord and the inner surface of the thyroid cartilage [6].
The Infant Larynx
The infant larynx differs from the adult larynx in several aspects. An accurate understanding of the anatomy and histopathology of the larynx is essential in treating causes of airway obstruction, such as congenital laryngeal stenosis, as well as incomplete development resulting in posterior laryngeal cleft.
Location
The infant larynx differs from the adult larynx in a few key aspects. In the infant larynx, the inferior margin of the cricoid cartilage is at the level of the fourth cervical vertebra (C4) and the tip of the epiglottis is at C1. The thyroid cartilage is within the arch of the hyoid bone and slightly inferior to it (fig. 2). This laryngeal positioning allows for the epiglottis to rest posterior to the soft palate, which permits simultaneous sucking and respiration contributing to the obligate nasal breathing of the newborn [7]. As one progresses through childhood, the cricoid cartilage descends to the level of C6 and then to the level of C7 in the adult.
Size
At birth, the infant larynx is approximately one third the size of the adult larynx. Several structures are relatively larger in the infant larynx (see fig. 4). The vocal processes of the arytenoids comprise slightly more than half the infant glottis, whereas in the adult, they comprise approximately one seventh to one fourth the length of the glottis [5]. The cuneiform cartilages, arytenoids, and soft tissue that comprise the posterior supraglottic larynx are larger in the infant. At endoscopy, the infant larynx appears anteriorly displaced, the arytenoids are prominent and the membranous portion of the vocal fields is short. At the level of the glottis, the vocal folds are 6-8 mm in length. The posterior glottis is approximately 3-4 mm in width. The subglottic larynx has a diameter of 5-7 mm; a diameter of 4 mm represents a subglottic stenosis [8]. A 3.5-mm endotracheal tube or a size 3 bronchoscope (5 mm outside diameter) should pass through the larynx of a newborn infant without substantial resistance. The superior margin of the first tracheal arch forms a ridge often prevalent at endoscopy.
Fig. 3.
Normal larynx of a 3-year-old boy. Tubular omegashaped epiglottis is noted.
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Configuration
The infant epiglottis is more narrow, posterior, and tubular or omega shaped when compared to the adult epiglottis (fig. 3). The lumen at the glottis is somewhat pentagonal in shape during inspiration. As the vocal folds taper inferiorly into the subglottic larynx, the lumen is elliptical, with the greater diameter in the anteroposterior dimension. At the inferior aspect of the cricoid cartilage, the lumen is round (fig. 4). When viewed in the coronal plane, the lumen is narrower at the top and wider at the bottom, resembling an inverted funnel. However, when viewed in the sagittal plane, the laryngeal lumen is slightly larger superiorly at the glottic level and narrower at the inferior aspect of the cricoid cartilage. Congenital cricoid abnormalities are commonly encountered and discussed in the section below titled ‘Congenital Laryngeal Stenosis’ [6].
Fig. 4.
Horizontal sections through the larynx of an 18-month-old child corresponding to the superior most section of the larynx at the apex of the epiglottis to the inferior most section at the inferior aspect of the cricoid cartilage (a-h, respectively). a Omega-shaped epiglottis. b Hyoid bone located anterior to the thyroid cartilage. c Saccule extends superiorly to this level. d Hyoid again noted to be anterior to the thyroid notch. e Saccule located between the false vocal fold and the inner lamina of the thyroid cartilage. f Superior section with V-shaped posterior cricoid cartilage. g Mid-section through cricoid cartilage with posterior V shape. h Inferior section through cricoid cartilage with a round shape. From Holinger L and others: Pediatric Laryngology and Bronchoesophagology, Lippincott-Raven, 1997.
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Tissue Consistency
Cartilage, muscle, and submucosal tissue are softer and more pliable in the infant larynx. Looser, less fibrous, submucosal tissue permits passive movement with respiration, and greater reaction and swelling with a more significant loss of lumen in inflammatory conditions [6].
Congenital Laryngeal Stenosis
Subglottic stenosis is one of the most common causes of airway obstruction. It can be categorized as either acquired or congenital, by clinical or anatomic characteristics, as well as by histopathology Acquired subglottic stenosis is narrowing of the subglottic airway secondary to a traumatic or inflammatory event, most commonly endotracheal tube intubation usually in association with laryngopharyngeal reflux and infection. Subglottic stenosis is considered congenital when there is no known cause of the narrowing. Congenital subglottic stenosis, the third most common congenital laryngeal anomaly following laryngomalacia and vocal fold paralysis, is highlighted in this section [6].
With regards to the histopathologic classification, subglottic stenosis can be further categorized as either cartilaginous or soft tissue in nature. Cartilaginous subglottic stenosis can involve either a cricoid cartilage deformity or a trapped first tracheal ring. The elliptic cricoid is the most frequently diagnosed abnormal shape resulting in congenital subglottic stenosis. The ellipse pattern is due to a transverse diameter that is shorter than the anterioposterior diameter, resulting in less than normal cross-sectional area. These measurements are equal in the normal larynx. The cricoid cartilage can also assume a flattened shape with a transverse diameter greater than the anterioposterior diameter. The flattened cricoid can be associated with a trapped first tracheal ring, which involves the first tracheal ring telescoping within the cricoid cartilage causing the airway to be narrowed [9].
Upon clinical evaluation, symptoms can vary from mild stridor to severe obstruction due to the extent of the stenosis. Patients with severe obstruction may have apneic episodes, suprasternal and subcostal retractions, dyspnea, and cyanosis. Patients with congenital subglottic stenosis, particularly younger than 6 months, can also present with recurrent or persistent croup. In such patients, the underlying congenital pathology may be exacerbated by reflux events or infection, and congenital stenosis must be considered.
Evaluation of congenital laryngeal stenosis in addition to a thorough history and physical examination includes flexible fiber-optic laryngoscopy and imaging. Direct laryngoscopy and rigid bronchoscopy are vital in the assessment of congenital stenosis and also allow examination for possible synchronous airway lesions. Treatment is individualized and depends upon the nature and severity of the stenosis as well as the patient's physical condition. In general, congenital subglottic stenosis causing 50% or greater airway obstruction (Meyer-Cotton grade II or greater) may require surgical intervention, which can either be external or endoscopic approaches to cricoid expansion described in greater detail in subsequent chapters with emphasis upon surgical technique [9].
Posterior Laryngeal Cleft
The congenital posterior laryngeal cleft is a rare condition and is characterized by the incomplete development of the tracheoesophageal septum. The incidence of laryngeal cleft is approximately 1 in 10,000-20,000 live births and is more common in boys than girls, with a ratio of 5:3 [10]. A higher incidence of laryngeal cleft is reported with Pallister-Hall and Opitz-Frias syndromes [11].
Stridor, choking, cyanosis, and signs of aspiration are typical manifestations in newborns with congenital posterior laryngeal clefts. The stridor is often inspiratory but can be expiratory when associated with tracheomalacia. Other conditions that should be kept in mind when considering posterior laryngeal cleft include esophageal stricture, TEF, cricopharyngeal spasm, laryngomalacia, gastroesophageal reflux, and vocal fold paralysis.
The diagnosis of laryngeal clefts includes a high index of suspicion along with a thorough history and physical examination. Microlaryngoscopy under general anesthesia remains the gold standard in diagnosing posterior laryngeal clefts. Palpation with a probe is essential to determine the type of laryngeal cleft. In 1989, Benjamin and Inglis [10] presented a classification system in which 4 types of clefts were described: type 1 is a supraglottic interarytenoid defect that extends inferiorly no further than the level of the true vocal folds; in type 2, the cricoid lamina is partially involved with extension of the cleft below the level of the true vocal folds; type 3 is a total cricoid cleft extending inferiorly with or without further extension in the cervical trachea; type 4 extends into the posterior wall of the thoracic trachea [11].
Treatment of posterior laryngeal clefts involves initial stabilization of the infant’s airway. The timing and approach for surgical repair depends on the severity of symptoms and the type of cleft present. Small clefts may be missed that often do not require surgical intervention. More significant clefts extending below the vocal folds are typically addressed via a cervical approach [6].
The Trachea and Bronchi
The anatomy of the normal tracheobronchial tree is presented in this section.
Trachea
The trachea extends from the inferior margin of the cricoid cartilage to the carina. The inferior end of the trachea is at the level of the fifth thoracic vertebra or the sternal angle. The trachea is 4 cm long in a full-term newborn infant and 11-13 cm long in an adult. The diameter of the trachea is 4-5 mm in a full-term newborn and 12-23 mm in an adult. The posterior or membranous portion of the trachea, or pars membranosa, is composed of the trachealis muscle and elastic and fibrous tissue. The ratio of cartilaginous to membranous trachea normally is 4.5:1. Variations in the tracheal cross-section diameter occur during breathing and coughing as a result of changes in head and neck position as well as intrathoracic pressure [12].
Bronchi
The trachea bifurcates at the carina, which is relatively acute in adults but less so in infants. The right main bronchus branches off at a 25° angle from the trachea, the left at a 45° [13]. Horseshoeshaped cartilages support the main bronchi. The right main bronchus is shorter but larger in diameter than the left. The right main bronchus is straight, whereas the left often has a gentle curvature.
In normal humans, there are three lobar bronchi on the right and two on the left. Usually, there are ten segmental bronchi on the right and eight on the left. The lobar bronchi most often are constant, but there is considerable variability in the segmental bronchi. Cartilage plates support the lobar, segmental, and smaller distal bronchi [14].
The right main bronchus branches into the upper lobe bronchus and the bronchus intermedius. The upper lobe bronchus divides into anterior, posterior, and apical segments. The bronchus intermedius divides into the middle lobe and lower lobe bronchi. The middle lobe bronchus divides into medial and lateral segments. The first branch of the lower lobe bronchus is the superior segment. The remainder of the lower lobe divides into medial, anterior, lateral and posterior basal segments.
The left main bronchus divides into upper and lower lobes. The upper lobe bronchus then divides into the upper division and the lingual. The upper division has anterior and apicoposterior segments. The lingual has superior and inferior segments. The first branch of the lower lobe is the superior segment. The three basilar segments of the left lower lobe are the anteromedial, lateral, and posterior basal segments [6].
Adjacent Vascular and Cardiac Anomalies
Knowledge of adjacent anatomy and vasculature becomes particularly important when assessing etiology of external compression of the tracheobronchial tree. Tracheomalacia is the abnormal narrowing of the tracheal walls, and is classified as primary or secondary. In primary tracheomalacia, the defect is intrinsic to the trachea. No extrinsic factors cause compression or distortion, and the cartilage-to-membranous trachea ratio may be 3 to 1, or even 2 to 1. The flattened posterior membranous trachea collapses forward during expiration (and more so with coughing), often touching the anterior wall. In secondary tracheomalacia, other factors are related to the pathology. Similarly, bronchomalacia is the abnormal narrowing of the bronchial walls, which can also be secondary to adjacent pathology. In particular, certain types of vascular and cardiac abnormalities are noted to cause specific presenting symptoms and characteristic endoscopic findings and are discussed below.
Fig. 5.
Endoscopic depiction of the tracheobronchial tree and typical findings secondary to adjacent vascular pathology and cardiovascular disease.
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Aberrant Innominate Artery
An aberrant innominate artery may cause compression of the trachea seen on endoscopy as compression of the right anterolateral wall of the upper trachea, giving the lumen a triangular shape (fig. 5). Lifting the tip of the bronchoscope against the pulsatile artery diminishes the right brachial pulse. This compression can lead to a variety of presenting symptoms, including a croupy or barky cough, wheezing, expiratory stridor, or apneic episodes. The differential diagnosis to be considered includes central apnea, gastroesophageal reflux with apnea, and other causes of apparent life-threatening events [6].
Patients with severe obstruction and subsequent life-threatening episodes, recurrent pneumonia due to ineffective clearance of secretions, and progressive obstruction may warrant suspension of the innominate artery and aorta to the posterior surface of the sternum (innominate arteriopexy). Yet, the majority of patients with an aberrant innominate artery resulting in extrinsic airway compression do not require surgical intervention due to its self-limiting nature.
Double Aortic Arch
The double aortic arch is a relatively rare congenital anomaly in which two aortic arches form a complete vascular ring that encircles the trachea and esophagus, forming a complete ring (fig. 5). Most commonly, there is a dominant right arch posterior and a hypoplastic left arch anterior to the trachea and esophagus. The two arches subsequently join the descending aorta, which is usually on the left side.
Symptoms related to this anomaly are due to the compression of the trachea and/or the esophagus and usually begin at birth. Diagnosis can often be suspected or made by radiograph, barium esophagram, or echocardiography. Computer tomography or magnetic resonance imaging are more specific and note the anatomic relationship of the aortic arches to the trachea and esophagus. This aids the cardiovascular surgeon in planning surgical division of the ring. Many patients experience almost immediate postoperative resolution of obstructive symptoms, whereas in some it takes 1-2 years for respiratory symptoms to improve [6].
Pulmonary Artery Sling
The pulmonary artery (PA) sling is associated with an absent left PA and is, instead, associated with an aberrant left PA arising from the right PA. Upon endoscopy, this vascular anomaly may cause compression of the right main bronchus, which may have a slit-like lumen and subsequently courses between the trachea and esophagus (fig. 5). The lower trachea is narrowed from the right side. Treatment includes surgery to divide and reimplant the artery, improving obstructive symptoms [15].
Congenital Cardiac Defects
Pulmonary hypertension secondary to a left-to-right shunt can lead to enlargement of the pulmonary arteries and subsequent compression of the left main bronchus (fig. 5). The left main bronchus normally traverses the superior aspect of the left atrium and left pulmonary veins, also passing adjacent to the pulmonary arteries. Patients with ventral septal defects or patent ductus arteriosus may have such compression secondary to left-to-right shunt and resulting pulmonary hypertension [15].
Symptoms depend upon the severity of airway obstruction and may include wheezing, recurrent pneumonia, atelectasis, or lobar emphysema. Severe cases may include ventilator dependence due to high mean airway pressures needed to overcome compressed airways. Bronchoscopy may yield left-sided bronchial compression. Computed tomography of the chest with contrast, magnetic resonance imaging, or cardiac catheterization may reveal the underlying pathology. Treatment is targeted towards relief of pulmonary hypertension and subsequent airway compression. PA plication or arteriopexy are rarely indicated [16].
Tracheoesophageal Fistula and Esophageal Atresia
A TEF is an abnormal connection between the esophagus and the trachea. Congenital EA results in two blind-ended pouches, an upper and a lower, which may or may not communicate with the tracheobronchial tree resulting in a TEF. Presenting symptoms include feeding and/or respiratory difficulties as well as persistent aspiration. TEF and EA occur in approximately 1 in 3,000-5,000 births. The five forms of EA and TEF are illustrated in figure 6. Treatment is surgical and involves primary extrapleural repair of EA with division and oversewing of the distal fistula. Postsurgical complications include tracheomalacia, esophageal stricture, recurrent fistula, and gastroesophageal reflux. The prognosis of surgical intervention is good, but respiratory complications may be severe [17].
Fig. 6.
Five types of EA and tracheoesophageal atresia. Type C is the most common.
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Conclusions
The pediatric airway endoscopist must be well versed in the normal and pathologic anatomic and developmental variations. Knowledge of key structural features involving the larynx, trachea and bronchi is essential in understanding the diagnosis and treatment of congenital laryngeal stenosis, posterior laryngeal cleft, external compression secondary to adjacent vascular and cardiac anomalies, as well as EA and TEF.
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References
Henick DH: Three dimensional analysis of murine laryngeal development. Ann Otol Rhinol Laryngol Suppl 1993;159:3-24
O'Rahilly R, Müller F: Chevalier Jackson lecture. Respiratory and alimentary relations in staged human embryos. New embryological data and congenital anomalies. Ann Otol Rhinol Laryngol 1984;93:421-429
Zaw-Tun HI: Development of congenital laryngeal atresias and cleft. Ann Otol Rhinol Laryngol 1988;97:353
Bosma JF: Anatomy of the Infant Head. Baltimore, The John Hopkins University Press 1985;
Hirano M, Kurita S, Kiyokawa K, Sato K: Posterior glottis. Morphological study in excised human larynges. Ann Otol Rhino Laryngol 1986;95:576-581
Holinger LD: Pediatric Laryngology & Bronchoesophagology. Philadelphia, Lippincott Raven 1997;
Holinger PH, Johnson KC, Schiller F: Congenital anomalies of the larynx. Ann Otol Rhino Laryngol 1954;63:581-606
Schild JA: Relationship of laryngeal dimensions to body size and gestational age in premature, neonates and small infants. Laryngoscope 1984;94:1284-1292
Schroeder JW, Holinger LD: Congenital laryngeal stenosis. Otol Clin North Am 2008;41:865-875
Benjamin B, Inglis A: Minor congenital laryngeal clefts: diagnosis and classification. Ann Otol Rhinol Laryngol 1989;98:417-420
William PL, Warwick R: Gray’s Anatomy ed 36Philadelphia, WB Saunders, 1980;1246
Hollinshead WH, Rosse C: Textbook of Anatomy ed 4Philadelphia, Harper & Row, 1985;494
(eds) Williams PL, Warwick R: Gray’s Anatomy ed 36Philadelphia, WB Saunders, 1980;1257
Landing BH, Dixon LG: Congenital malformations and genetic disorders of the respiratory tract. Am Rev Respir Dis 1979;120:151-185
Holinger PH: Congenital anomalies of the tracheobronchial tree. Postgrad Med 1964;26:454-462
Benjamin B, Pham T: Diagnosis of H-type tracheoesophageal fistula. J Pediatr Surg 1991;26:667-671
Benjamin B: Endoscopy in esophageal atresia and tracheoesophageal fistula. Ann Otol Rhinol Laryngol 1981;90:376
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