Basic Airway Anatomy of the Pediatric Patient

Anatomy of the pediatric airway

The airway extends from the external nares to the junction of larynx to the trachea; it includes nose, the paranasal sinuses, the pharynx and the larynx.

Nose

The external nose is made u of the nasal bones, the nasal part of the frontal bones and the frontal processes of the maxillae. The nasal cavity is divided by the nasal septum in two compartments that open to the exterior via the nares and into the nasopharinx via the choanae. In a child, the nose is soft and distensible, with relatively more mucosa and lymphoid tissue than in the adult. In children, the small nasal apertures are easily obstructed by secretions, edema or blood. As infants are obligate nasal breathers, such conditions may increase the work of breathing, and similarly contribute to difficulties with management of the airway during general anaesthesia.

Paranasal sinuses

The ethmoidal and maxillary sinuses are present at birth. The frontal sinuses develop later. The sphenoid sinuses develop late in childhood and are not significant until adolescence. Sinusitis may lead to airway obstruction due to secretions. Cellulitis, edema or abscesses may also occur.

Pharynx

The pharynx is in communication with the nasal cavity, the mouth and the larynx.

Nasopharynx

The nasopharynx lies behind the nasal cavity and above the soft palate. During development, the depth of the nasopharynx increases as a result of remodeling the palate as well as changes in angulation of the skull base, eventually producing an enlarged nasal airway in the adult. The pharyngeal opening of the pharyngotimpanic tube lies in the nasopharinx. The nasopharyngeal tonsils (adenoids) lie on the roof and posterior wall of the nasopharynx in children. The enlargement in early childhood may obstruct breathing through the nose.

Oropharynx

The oropharynx extends from the soft palate to the tip of the epiglottis. It is attached anteriorly to the base of the tongue via the glossoepiglottic folds. Between these folds lie the valleculae. The sensory innervation of the oropharynx is derived from the glossopharyngeal nerve and the superior laryngeal branch of the vagus nerve, which transmits afferent impulses from the base of the tongue and the valleculae. The reflex circulatory responses to direct laryngoscopy and tracheal intubation result largely from stimulation of the pharyngeal wall by the laryngoscope blade. At the entrance of the oropharynx is a collection of lymphoid tissue known as Waldeyer’s ring. It consists of the lingual tonsils at the base of the tongue and bilateral palatine tonsils. Inflammation of these tissues may obstruct breathing efforts in conscious patients and male laryngoscopy difficult because of an increase in size of the tissue. The relatively large tongue decreases the size of the oral cavity in children and more easily obstructs the airway. Decreased muscle tone also contributes to passive obstruction of the airway by the tongue. In infants lying supine, the tongue tends to flatten out against the soft palate in inspiration and may remain in the same position for the passive expiration through the nose. Extension of the head at the atlanto-occipital joint, with anterior displacement of the cervical spine, may result in improved airway patency but does not necessarily change the position of the tongue.

Laryngopharynx

The laryngopharynx extends from the tip of the epiglottis to the lower border of the cricoid ring. The larynx bulges back into the center of the laryngopharynx, leaving a recess on either side, known as the piriform fossa.

Larynx

The larynx is situated between the pharynx and the trachea, extending from the base of the tongue to the cricoid cartilage. It is the organ of phonation. The development of the respiratory system begins at three weeks of gestational age; a definite larynx can be identified by 41 days of gestation. The cricoid and thyroid cartilages begin condrification at 7 weeks. The primitive glottis is formed at 10 weeks gestation when the vocal cords split. Failure of this process results in a congenital laryngeal web, or in some cases, congenital atresia of the larynx. Incomplete division of the embryonic foregut into the anteriorly positioned trachea and the posteriorly positioned esophagus results in tracheo-oesophageal fistula.

The larynx consists of the thyroid cartilage, the cricoid cartilage, the paired arytenoids and the epiglottis, together with the small corniculate and cuneiform cartilages. The largest of these cartilages is the thyroid cartilage, which is open posteriorly and forms the laryngeal prominence (Adam’s apple) anteriorly. Beneath the thyroid cartilage is the cricoid cartilage, in the shape of a signet ring with the widest portion lying posteriorly. This is the only complete cartilage ring found in the respiratory tract. At birth, the lower border of the cricoid cartilage lies opposite the lower border of the fourth cervical vertebra. At 6 years of age it is at the level of the fifth cervical vertebra and in the adult it lies at the level of the sixth cervical vertebra. Because of the small size of the cricoid cartilage in children, and the fact that it is a complete ring, the presence of mucosal edema at this site will severely compromise the airway. Young children are also at risk of acquired subglottic stenosis when exposed to prolonged or repeated tracheal intubation.

The vestibular folds, or false cords, are created by the mucosa that covers the thyroarytenoid muscles. The true vocal cords are the vocal folds covered by mucosa. Reflex adduction of the true and false cords is known as laryngospasm and may result from local stimulation of the larynx, or from surgical stimulation in the absence of adequate anesthesia. The cricothyroid membrane is a tough, elastic connective tissue sheet that spans the joint between the inferior process of the thyroid cartilage and the cricoid cartilage. Puncture or incision of this membrane allows the creation of a surgical airway when acute airway obstruction occurs at or above the larynx.

The epiglottis is a leaf-shaped structure attached to the posterior border of the thyroid cartilage by the thyroepiglottic ligament. In the adult, the epiglottis is broad, with its axis parallel to that of the trachea. The epiglottis in the infant is narrower, softer and more horizontally positioned than in the adult. At laryngoscopy, the epiglottis in the neonate appears more deeply furrowed at its free end, and in some babies it has a V-shaped appearance.

The more superior location of the larynx in children may create difficulty in visualizing laryngeal structures because of the more acute angulation between the base of the tongue and the laryngeal opening (4). During laryngoscopy, a neck or shoulder roll will relieve the hyperflexion of the infant’s neck caused by the relatively large occiput.

The nerve supply to the larynx is from the vagus nerve, via its superior and recurrent laryngeal branches. The superior laryngeal nerve gives rise to an internal laryngeal branch which runs beneath the mucosa of the piriform fossa. In this position, it is easily blocked by the topical application of a local anesthetic agent to provide anesthesia for laryngoscopy and bronchoscopy. The laryngeal inlet and the inferior surface of the epiglottis are innervated by the vagus nerve. When the epiglottis is lifted with a straight laryngoscope blade, bradycardia and hypotension may occur as a result of a vagal reflex. When a curved blade is used, the tip is placed in the angle between the epiglottis and the base of the tongue. This theoretically reduces the risk of bradycardia because the superior surface of the epiglottis and the valleculae are innervated by the glossopharyngeal nerve. Damage to the recurrent laryngeal nerve results in paralysis of the corresponding vocal cord, causing it to lie motionless in the midline and at a lower level than the opposite side. Bilateral paralysis results in complete loss of vocal power. The two paralyzed cords may then flap together to cause a valve-like obstruction during inspiration, producing dyspnea and inspiratory stridor.

The pediatric airway is highly compliant and the cartilaginous support is less developed than in the adult airway. This leads to increased susceptibility to dynamic airway collapse in the presence of airway obstruction. Loss of muscle tone in the pharynx leads to airway obstruction at the level of the soft palate and epiglottis. Laryngomalacia is a congenital abnormality of the larynx and results from the laryngeal structures being more pliable and less rigid than in the adult.

History

Begin inquiring about the child’s medical history, including details of the birth and subsequent development, previous respiratory illnesses, history of any injuries or surgical procedures to the airway. Details should be taken about any complications occurring during previous anesthetics and questions should be asked about the child’s respiration, feeding and phonation as well as presence of cough.

Noisy breathing signifies abnormalities within the pediatric airway. Enlarged adenoids and tonsils are associated with snoring and hyponasal speech.A history of cessation of sleep or excessive daytime somnolence may be suggestive of obstructive sleep apnoea. Episodes of apnoea may also be of central origin, as can occur in association with prematurity. Abnormal feeding patterns occur with respiratory insufficiency in the infant, particularly when associated with aspiration, as suggested by choking, coughing and vomiting.

Ask about the child’s voice or cry; hoarseness or diminished cry are signs of laryngomalacia; changes in quality of the voice occur also in unilateral vocal cord paralysis. Cough is a common symptom, often associated with upper respiratory tract infection; in this case it is associated with purulent nasal secretion. A croup-like cough in absence of infection may signify subglottic stenosis. Sudden onset of cough in the absence of systemic illness suggests inhalation of a foreign body.

Examination

Assess the general appearance of the child with particular reference to body mass index and characteristics of the face. Failure to thrive is a recognized consequence of obstructive sleep disorder, particularly when it is caused by adenotonsillar hypertrophy. Abnormalities of the airway have been described in obese children.

The child’s facial expression or the presence of nasal flaring may suggest respiratory distress. Mouth-breathing or drooling often occur with enlarged tonsils or adenoids. There may be signs of previous trauma or surgery to the head and neck. Note evidence of neuromuscular disease, congenital abnormalities, dysmorphic features as well as mandibular hypoplasia, small mouth or limited mouth opening. Macroglossia and retrocline of lower incisors are associated with sleep apnea.

Examination of the neck may reveal deformity limited motility of the cervical spine or cervical lymphoadenopathy. The shape of the chest should be observed and lungs should be auscultated. Hoarseness or a weak cry may occur with airway obstruction at the level of the vocal cords. Stridor is a high-pitched sound indicative of laryngeal or tracheal obstruction; inspiratory stridor suggests obstruction at the above trachea because extrathoracic obstruction is exacerbated by the negative intrathoracic pressures generated in inspiration. Expiratory stridor suggests obstruction of the lower trachea or bronchi, with exacerbation when the airways are compressed during forced expiration.

In laryngomalacia, excessive flaccidity of the soft epiglottis and the loose aryepiglottic folds causes these structures to collapse on inspiration, resulting in stridor. This collapse is exaggerated on crying because the inspiratory effort is greater, leading to increased collapse of the soft supraglottic structures. Inhalation induction of anesthesia often leads to a decrease in the stridor of laryngomalacia, because of a reduction in the force of respiratory movements.

Difficult airway prediction

The airway evaluation needs to include the patient’s medical history: birth complications, history of trauma, previous surgery, and airway management during previous anesthesia. During the clinical examination, the anesthesiologist should seek for signs of stridor, dysphonia, swallowing disorders, difficulty in breathing, difficulty in speaking, and hoarseness. There are currently a number of difficult airway predictors, but their sensitivity and specificity vary in clinical practice. The predictors with good performance are mandibular protrusion, Mallampati’s classification, movement of atlanto-occipital joint, reduced mandibular space, and increased tongue thickness. Other published risk factors are age less than one year, ASA (American Society of Anesthesiologists) status III and IV, obesity (BMI, body mass index, ≥35), and patients undergoing oromaxillofacial, ENT (ear, nose, and throat), and cardiac surgery. The thyromental distance can be used for difficult airway prediction: the normal value should be at least 3 finger breadths (patient’s 3 finger breadths). The reported incidence of difficult airway in pediatric population however is lower than that for adults and predictable in the majority. Unexpected difficult face mask ventilation (inadequate mask seal, excessive gas leak, or excessive resistance) in children varies from 2.8 to 6.6% [8] and the incidence of difficult endotracheal intubation (defined as Cormack and Lehane greater than grade 3) varies between 0.06% and 1.34%. Difficult airway should be anticipated in several congenital syndromes: Pierre robin sequence, Goldenhar syndrome, Treacher Collins syndrome, Apart syndrome, Hunter and Hurlet syndrome, Backwith- Wiedermann syndrome, Freeman-Sheldon syndrome, Down syndrome, Klippel-Fail syndrome, Hallermann-Strei syndrome, Arthrogryposis, Cri-du-chat syndrome, Edwards syndrome, and Fibrodysplasia ossificans progressiva.