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

Level	Newborn	Older infant and child
Nasal	Choanal atresia
Oropharyngeal	Facial malformations (e.g. Pierre Robin syndrome, Treacher Collins syndrome)	Macroglossia/postglossectomyAngioedema
	Macroglossia	Retropharyngeal abscess
	Cystic hygroma	Tonsillar and adenoidal hypertrophy
	Vallecular cyst	Obstructive sleep apnoea
Laryngeal	Infantile larynx	Acute laryngotracheobronchitis (croup)
	Bilateral vocal cord palsy	Bacterial tracheitis
	Congenital subglottic stenosis	Acute epiglottitis
	Subglottic haemangioma	Postintubation oedema and stenosis
	Laryngeal web	Laryngeal papillomata
	Laryngeal cysts	Laryngeal foreign body
		Inhalation burns
		Caustic ingestion
		External trauma
Tracheal	Tracheomalacia	Foreign body
Tracheal	Vascular ring	Anterior mediastinal tumours (e.g. lymphoma)

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

EPIGLOTTITIS

Epiglottitis is a life-threatening supraglottic lesion which, prior to vaccination, was caused almost exclusively by Haemophilus influenzae type b. The prevalence of epiglottitis has fallen dramatically with the uptake of H. influenzae vaccination. It still occurs due to failure to vaccinate or vaccine failure. Occasional cases are caused by Streptococcus, Staphylococcus, Pneumococcus and Meningococcus, as well as by viruses. Non-infective causes include corrosive ingestion and thermal injury.

The diagnosis is usually obvious from history and clinical features. There is an acute onset of high fever, toxaemia and noisy breathing. The child adopts a characteristic posture, preferring to sit with mouth open, drooling saliva. The tongue is often proptosed and immobile. Cough is usually absent. These features are the legacy of an intensely painful pharynx. Due to the accompanying septicaemia, the severity of illness often appears out of proportion to the degree of airway obstruction. Typically, a low-pitched inspiratory stridor is present, accompanied by a characteristic expiratory snore. Atypical cases with cough and without fever may obscure the diagnosis.

Sudden total obstruction is not infrequent, and may be precipitated by examination of the pharynx, by placing the child in the supine position or stressful procedures (e.g. cannula insertion). When the diagnosis is in doubt, a lateral X-ray of the neck in the sitting position should be taken in the emergency department or ICU, provided that staff capable of securing the airway remain in attendance. Examination of the pharynx must not be undertaken unless personnel and facilities are available for immediate intubation.

MANAGEMENT

PARENTERAL ANTIBIOTICS

Third-generation cephalosporins are the preferred antibiotics because of emerging resistance to ampicillin and, to a lesser extent, chloramphenicol. Appropriate regimens include cefotaxime 200 mg/kg per day i.v. for 5 days, or ceftriaxone 100 mg/kg i.v. statim followed by 50 mg/kg i.v. after 24 hours. Co-trimoxazole is usually an effective enteral antibiotic if more prolonged therapy is required.

RELIEF OF AIRWAY OBSTRUCTION

All but the mildest cases require insertion of an artificial airway under anaesthesia (see below). Nasotracheal intubation is the optimal management,¹¹ although, depending on the available personnel, tracheostomy is a satisfactory alternative. Anaesthesia for relief of airway obstruction is described below. A tube of size appropriate for age is chosen (see Chapter 104). Extubation can be undertaken when fever subsides and the child no longer appears toxic. Most cases can be extubated in less than 18 hours. Only those complicated by pulmonary oedema, pneumonia or cerebral hypoxia (from delayed therapy) will require intubation for longer than 24 hours. It is not necessary to re-examine the larynx prior to extubation. Nebulised adrenaline (epinephrine) is of no benefit in this condition and may aggravate the situation.¹² Pulmonary oedema, when it occurs, is due to airway obstruction, septicaemia and increased lung capillary permeability.^3,^13,¹⁴ It is managed according to conventional principles.