ANATOMICAL DIFFERENCES AND CLINICAL RELEVANCE

Differences in the anatomy and function of the airway are important considerations in airway maintenance, laryngoscopy and intubation. In the newborn, the nose contributes approximately 42% of total airways resistance, which is considerably less than the adult’s 63%. Thus, infants are obligatory nose-breathers. The epiglottis is longer, U-shaped and floppy, and may need to be lifted with a straight-bladed laryngoscope for visualisation of the larynx and intubation. The larynx is higher in the neck (C3–4) in the neonate, and has an anterior inclination.¹ It descends over the first 3 years of life, and again at puberty, to ultimately lie opposite C6. The length of the trachea varies from 3.2 to 7.0 cm in babies weighing less than 6 kg. Accurate positioning of the tracheal tubes is required to prevent accidental extubation or endobronchial intubation. The narrowest part of the airway until puberty is the cricoid ring. This part of the airway is most vulnerable to trauma and swelling. The narrow cricoid ring also dictates tube size, and allows use of uncuffed tubes in infants and children.

PATHOPHYSIOLOGY

Although the ratio of airway diameter to body weight is relatively large in the infant, in absolute terms airway diameter is small, and a minimal reduction causes a devastating increase in airway resistance. For example, the diameter of the newborn’s cricoid ring is 5 mm. A 50% reduction in radius will result in turbulent flow, and increases the pressure (and work) required to maintain breathing 32-fold.²

Symptoms and signs vary with the level of obstruction, the aetiology and the age of the child. Airway obstruction may be extrathoracic, intrathoracic or a combination. Extrathoracic obstruction is more pronounced during inspiration and is characterised by inspiratory stridor and prolongation of inspiration. Intrathoracic obstruction affecting either large or small airways is more pronounced during expiration and is characterised by expiratory stridor, prolonged expiration, wheeze and air trapping. Biphasic stridor is characteristic of mid tracheal lesions. These features mirror the intrapleural and airway pressure changes of the respiratory cycle (Figure 97.1). Retraction of the chest wall, an important sign of respiratory distress, reflects the negative intrapleural pressures generated combined with the compliance of the chest wall. Large negative intrapleural pressures are also transmitted to the interstitium of the lung, and may result in pulmonary oedema.^3,4 Cor pulmonale may develop secondary to chronic obstruction, hypoxia and pulmonary hypertension.^5,6

Figure 97.1 Dynamics of (a) extrathoracic and (b) intrathoracic airways obstruction.

CLINICAL PRESENTATION

Stridor is noisy breathing due to turbulent air flow. It is the cardinal feature of URTO. Parents complain that their child has noisy breathing and of ‘sucking the chest in’. The pitch and timing of stridor provide information about the degree and level of obstruction.

Voice sounds may also be informative. Nasal obstruction results in hyponasality. Oropharyngeal obstruction may cause a ‘hot potato’ voice. Supraglottic obstruction is characterised by a muffled voice. Children with glottic lesions may be hoarse or aphonic.

Retraction of the chest wall develops as obstruction progresses. Retraction is less prominent in older children, as the chest wall is more stable. As obstruction worsens, the work of breathing increases and the accessory muscles become active. The alae nasi (vestigial muscles of ventilation) begin to flare. Fever increases minute volume and magnifies any degree of obstruction. Whereas infants and older children can maintain an increased work of breathing, premature infants and neonates rapidly fatigue, and may develop apnoeic episodes.^7,8

Auscultation over the neck and larynx may identify the site of obstruction. A foreign body in the airway may produce a mechanical or slapping sound. Decreased or absent breath sounds may occur with greater degrees of obstruction. Chronic URTO is a cause of failure to thrive, chest deformity (pectus excavatum) and cor pulmonale.^5,6 Some infants present with recurrent chest infections. Abnormal posturing (head retraction) may also be a feature, particularly in infants.

Initially, the child with airway obstruction exhibits tachypnoea and tachycardia. If obstruction is severe and persistent, exhaustion eventually occurs, and the child exhibits decreased respiratory effort, decreased stridor and breath sounds, restlessness, cyanosis, pallor and eventually bradycardia.

AETIOLOGY

A classification of the causes of URTO is presented in Table 97.1. The neonatal causes are predominantly due to congenital structural lesions. Acute inflammatory lesions, foreign bodies and trauma predominate in older infants and children.

Table 97.1 Causes of upper airway obstruction in children

DIAGNOSIS

The cause of URTO can often be determined from the history and clinical features. Radiographic examination of the upper and lower airways with anteroposterior and lateral views may show soft-tissue swelling or the presence of foreign bodies.⁹ Air shadows may indicate fixed stenotic or compressive lesions. In children with significant respiratory distress, these investigations should be undertaken in the intensive care unit (ICU) rather than the radiology department.

Previously, barium swallow and aortography have been used to confirm the diagnosis of vascular compression of the trachea. Computed tomography (CT) has assumed importance in the assessment of fixed lesions such as intrinsic stenosis and extrinsic compression. Echocardiography, magnetic resonance imaging (MRI) and CT with contrast are useful to assess vascular anomalies.¹⁰ Tracheobronchography may provide excellent anatomical delineation of the proximal tracheobronchial tree and allow dynamic assessment of airway calibre.

Direct visualisation of the airway may be necessary, and may also prove therapeutic (e.g. removal of a foreign body). Nasoscopy, flexible fibreoptic and rigid laryngoscopy and bronchoscopy all have a place in assessing the paediatric airway. Investigation of the child’s airway should only be undertaken in specialised centres by experienced endoscopists, radiologists and anaesthetists.

Blood gas determination is rarely useful in assessment or monitoring of URTO. An exception to this is in very young infants where hypercapnic respiratory failure may occur early and insidiously in URTO. It is dangerous practice to await respiratory failure before intervention. Mild hypoxaemia only may be present until fatigue, hypoventilation, cyanosis and hypercapnia occur. Pulse oximetry may provide useful warning information. An oxygen saturation less than 90% in a patient with pure URTO (without lung disease) is a reason for concern.

SPECIFIC AIRWAY OBSTRUCTION