Upper respiratory tract obstruction in children

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Chapter 97 Upper respiratory tract obstruction in children

Alan W. Duncan

Upper respiratory tract obstruction (URTO) is a common cause of respiratory failure in infants and children. This reflects the frequency of upper respiratory tract abnormalities and disorders, the presence of narrow airways and the structural inefficiencies of the lung and chest wall. The majority of children with critical airway obstruction are otherwise healthy, and expert management results in a normal life expectancy. Poor management can lead to cardiopulmonary arrest and hypoxic cerebral damage.

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

image

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
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.

PROPHYLAXIS

Most invasive infections due to H. influenzae occur in children under 5 years of age. The risk of infection in close contacts is about 500-fold higher than in the general population. It is thus recommended that all members (including adults) of any household with H. influenzae type b infection and with another child under 4 years should be given prophylactic antibiotics. An accepted regimen is oral rifampicin 20 mg/kg per day (maximum 600 mg) for 4 days. An alternative is a single dose of ceftriaxone 100 mg/kg i.m. or i.v.

CROUP

Croup or acute laryngotracheobronchitis is due to inflammation and oedema of the glottic and subglottic regions. The narrowest part of the child’s upper airway is the subglottic region, the point at which critical narrowing occurs. Retained secretions due to the bronchitic component may compound the obstruction. Croup is uncommon in children under 6 months of age, and an underlying structural lesion such as subglottic stenosis or haemangioma with superimposed infection should be suspected. Endoscopy is warranted if the child has a prior history of stridor or if symptoms persist beyond the acute episode.

Three subgroups are recognised: viral croup, spasmodic croup and bacterial tracheitis.

VIRAL CROUP

Viral croup, most commonly due to parainfluenza virus, respiratory syncytial virus and rhinovirus, is characterised by a coryzal prodrome, low-grade fever, harsh barking (croupy) cough and hoarse voice. Progression of airway obstruction in severe cases is shown in Figure 97.2.

image

Figure 97.2 Features of progressive upper-airway obstruction.

SPASMODIC CROUP

Spasmodic or recurrent croup occurs in children with an allergic predisposition.15,16 It usually develops suddenly, often at night, and without prodromal symptoms. Endoscopy reveals pale, watery oedema of the subglottic mucosa. Such children probably represent part of the asthma spectrum, and wheeze, due to small airway flow limitation, may be a feature.

BACTERIAL TRACHEITIS

Bacterial tracheitis is uncommon but should be suspected in children exhibiting the usual features of croup, but accompanied by high fever, leukocytosis and copious purulent secretions.17 There is a greater risk of sudden, severe obstruction from purulent secretions. Staphylococcus aureus is usually the cause, although H. influenzae and group A Streptococcus have also been isolated in some cases.

MANAGEMENT

Minimal disturbance is important, as restlessness will increase minute ventilation, oxygen consumption and signs of obstruction.

Adequate hydration: oral fluid intake must be encouraged to avoid dehydration. Nasogastric feeding is contraindicated, and i.v. fluids may occasionally be necessary. Overhydration must also be avoided. Hyponatraemia and convulsions due to inappropriate antidiuretic hormone secretion have been observed with prolonged, severe airway obstruction.

Oxygen therapy may mask signs of respiratory failure, but should be given to treat hypoxaemia. Its use can be guided by pulse oximetry (i.e. keep SaO2 > 90%). Oxygen administration may further stress the young child. The need for oxygen therapy is often an indication that the child is progressing towards intubation.

Corticosteroids have dramatically reduced the need for intubation in children with croup. They are effective in both viral and spasmodic croup.18,19 Steroids will also shorten the duration of intubation and increase the success rate of extubation.20,21 The dose of dexamethasone is 0.6 mg/kg statim (maximum dose 10 mg) followed, if necessary, by 0.15 mg/kg 6-hourly. In very distressed children, it is best administered i.m. or i.v. to ensure absorption. Inhaled steroids are also effective in milder cases.22

Humidification of inspired gases was the mainstay of supportive care for decades. Controlled studies showing efficacy are lacking. A study by Bourchier et al. failed to demonstrate benefit and its use has been abandoned in many centres.23

Nebulised adrenaline will usually provide temporary relief of acute obstruction.24 Historically, racemic adrenaline (2.25% solution, i.e. 1:88 L-adrenaline), developed for use in asthma, was employed. Indications for adrenaline nebulisation are:

• acute laryngotracheobronchitis, where relief usually lasts 1–2 hours, but may be longer if it facilitates secretions to be expelled. It is debatable whether the natural history of the disease is altered. It is an effective temporising measure until steroids have time to work. If given prior to induction, it will facilitate inhalational anaesthesia for intubation
• spasmodic croup, where one or two inhalations may produce lasting relief of airway obstruction
• post endoscopy or intubation oedema, where the benefit is often dramatic
• during transport, where administration may render the child safe for interhospital transfer without intubation

The empirical dose of racemic adrenaline is 0.05 ml/kg diluted to 2 ml with saline and nebulised with oxygen. The same dose of a strong preparation (1%) of the L-isomer can also be used. The same mass of L-adrenaline is also provided by 0.5 ml/kg (max 5 ml) of the standard 1:1000 solution of adrenaline, and this is equally effective. Antibiotics are indicated only for bacterial tracheitis where anti-staphylococcal cover is recommended.

Mechanical relief of airway obstruction: this requirement has been greatly reduced by early use of steroids. Increasing tachycardia, tachypnoea and restlessness indicate the need for tracheal intubation. An SaO2 persistently less than 90% is another reason for concern. It is important not to wait for the development of bradycardia, bradypnoea, cyanosis, exhaustion and respiratory failure. Blood gases are not a useful guide for intubation. Nasotracheal intubation is preferred. An orotracheal tube, size (inner diameter) 1 mm less than that predicted by age (Table 97.2) is first inserted under anaesthesia (see below). A stylet through the tube is recommended to overcome the resistance of the subglottic region. The tube is changed to a nasotracheal tube immediately after clearance of secretions.

Table 97.2 Nasotracheal tube size in croup

Age Size
Less than 6 months 3.0 mm
6 months to 2 years 3.5 mm
2–5 years 4.0 mm
Over 5 years 4.5 mm

Extubation can be performed when the child is afebrile, secretions have diminished and a leak is audible around the tube with coughing or application of positive pressure (25 cmH2O or less). The duration of intubation averages 5 days. Children under 1 year have a higher incidence of requiring intubation and a longer duration of intubation. Reintubation may be required in some cases. Endoscopy should be performed in cases that require repeated intubation to exclude underlying lesions and subglottic injury. Tracheostomy is a suitable alternative for some situations, although complications are more significant.

OTHER SUPRAGLOTTIC LESIONS

Retropharyngeal abscess, tonsillitis, peritonsillar abscess, infectious mononucleosis and Ludwig’s angina may all mimic epiglottitis. Local features will usually indicate the diagnosis. A retropharyngeal abscess can be detected by palpation and is obvious on a lateral X-ray of the neck. Airway relief, antibiotics, drainage and, rarely, neck incision form the basis of treatment for these disorders. A nasopharyngeal tube will provide relief of obstruction in most supraglottic lesions. In an emergency situation, placement of a laryngeal mask airway may be life-saving. Tonsillectomy, although best performed electively, is occasionally indicated in the acute phase of tonsillar obstruction. Steroids appear to be effective in reducing cervical lymphadenopathy and tonsillar enlargement in cases of infectious mononucleosis and the response is rapid.

TONSILLAR AND ADENOIDAL AIRWAY OBSTRUCTION

The contemporary conservative surgical approach to tonsillectomy and adenoidectomy has led to an increased incidence of hypertrophy and untreated chronic upper-airway obstruction.25 Such children may present with severe, acute exacerbations due to intercurrent infection (e.g. tonsillitis). They may present in a toxic state with drooling, thereby mimicking acute epiglottitis. Obstruction is most marked during sleep. In the most severe cases, it may be necessary to relieve the obstruction with a nasotracheal tube or a nasopharyngeal tube positioned beyond the tonsillar bed. Tonsillectomy and adenoidectomy are generally contraindicated in the acute phase, because of increased risk of bleeding, but are performed when infection has settled.

OBSTRUCTIVE SLEEP APNOEA SYNDROME

Obstructive sleep apnoea (OSA) syndrome is characterised by intermittent upper-airway obstruction during sleep, with heavy snoring, stertorous breathing and an abnormal, irregular respiratory pattern.26 Frequent episodes of chest-wall motion with inadequate airflow (hypopnoea) or absent airflow (obstructive apnoea) are a feature. These episodes are most frequent during rapid eye movement sleep. They are accompanied by variable degrees of oxygen desaturation. OSA may be associated with enlarged tonsils and adenoids, a large uvula or long soft palate, macroglossia, retrognathia or various neurological disorders. Obesity is a common finding.

If OSA is severe and protracted, cardiac and pulmonary decompensation may occur. Chronic hypoxia and hypercarbia lead to pulmonary hypertension and cor pulmonale.5,6 There may also be evidence of left ventricular failure and pulmonary oedema. Urgency of treatment is dictated by the mode of presentation. Critically ill children may require immediate relief of airway obstruction (nasopharyngeal or nasotracheal tube), oxygen therapy and diuretics. Antibiotics are indicated if there is bacterial superinfection. Surgical intervention is required after stabilisation. Tonsillectomy and adenoidectomy are often dramatically beneficial. They are best removed even when not grossly enlarged. Postoperative observation in a paediatric ICU or high-dependency unit is required for those with severe OSA. Other surgical procedures, such as uvulopalatopharyngoplasty or tracheostomy, may be required when this fails. The use of nocturnal continuous positive airway pressure (CPAP) is an option in long-standing, refractory conditions, e.g. neurological disorders. It is often not feasible because it is difficult to interface CPAP masks in young and uncooperative children.

PIERRE ROBIN SYNDROME

This sequence consists of a posterior cleft palate, retrognathia and relative macroglossia. It is the cause of airway obstruction, feeding difficulties and failure to thrive in the newborn. Differential growth eventually reduces the significance of the deformity. Acute airway obstruction may be relieved by nursing the infant in the prone position, by passage of a nasopharyngeal tube or insertion of a laryngeal mask airway.27 Occasionally, nasotracheal intubation or tracheostomy is required. Tongue–lip anastomosis has been used in the past but is now rarely performed.

CYSTIC HYGROMA

Although often conspicuous at birth, cystic hygroma is a relatively rare cause of upper-airway obstruction in infancy. The tumours consist of masses of dilated lymphatic channels. They usually occur in the neck and may involve tissues of the tongue and larynx. Occasionally, extension into the mediastinum occurs. Airway obstruction may be due to infection or haemorrhage into the lesion. Surgical excision has been the mainstay of treatment, although complete removal is difficult and recurrence is common. Treatment using sclerosing therapy is now used. Compounds used include bleomycin emulsion or OK 432.28,29 OK 432 is produced by lyophilisation of cultures of a low virulent strain of group A Streptococcus pyogenes (human origin). In severe cases, long-term tracheostomy is required.

INHALATION BURNS

Inhalational injury should be suspected with burns occurring in a closed space, and when facial burns, singed nasal hairs and oropharyngeal carbonaceous material are present. Respiratory complications are the major cause of mortality in children who are burnt. Direct airway burns or inhalation of products of combustion may lead to rapidly progressive oedema. The situation may be compounded by small airway and lung injury and by the need to provide adequate analgesia. Early intubation is strongly recommended prior to an emergency situation developing. Tracheal tube fixation is critical and may be problematic with extensive facial burns; it may require suturing of the tube to the nasal septum.

SUBGLOTTIC STENOSIS

Neonates with congenital subglottic stenosis may present with severe obstruction requiring intubation at birth. Other infants present with persistent stridor or recurrent croup due to superimposed infection. Subglottic stenosis may also occur as a complication of prolonged or traumatic intubation, the result of tube pressure, mucosal ischaemia and healing by fibrosis. Prolonged intubation or tracheostomy may be required. Surgical techniques such as the cricoid split procedure or laryngotracheoplasty may be required to enlarge the airway.

SUBGLOTTIC HAEMANGIOMA

Haemangiomata are common in infancy and occur in many parts of the body. Subglottic lesions often present in the second or third month of life and owe their importance to the anatomical location. Stridor is usually both inspiratory and expiratory. A hoarse cry is indicative of vocal cord involvement. Obstruction may be severe and is aggravated by crying, struggling or superimposed infection. Cutaneous haemangiomata are seen in 50% and, if present, provide a clue to diagnosis. Definitive diagnosis rests on endoscopy. The natural history is of spontaneous resolution between the first and second years of life. Meanwhile, tracheostomy or periods of intubation may be indicated to cover episodes of obstruction. Encouraging results are being obtained with laser surgery. Intralesional injection of steroids may be of benefit.

FOREIGN BODY OR CHOKING

A foreign body must be suspected in any acute obstruction occurring in an infant or child between 6 months and 2 years of age. Older children with neurological impairment are also at risk. A foreign body lodged in the pharynx results in gagging, respiratory distress and facial congestion. Laryngeal impaction usually produces stridor, a distressing cough and aphonia. Sudden total obstruction may occur. Symptoms usually develop while the child is playing or eating.

The technique for removal of a pharyngolaryngeal foreign body without equipment in infants and children is controversial and difficult. The American Academy of Paediatrics has made recommendations to cover various ages.30 Gravity should be utilised by placing the child prone, straddled over the arm with the head down and a hand supporting the jaw. Four back blows between the shoulder blades should be administered. If this fails, chest thrusts or finger sweep across the pharynx should be attempted. There is some risk that the latter manoeuvre may impact the foreign body in the larynx. Abdominal thrusts (the Heimlich manoeuvre) are not recommended in infants but may be useful in children older than 1 year. Expired air resuscitation should be attempted in an emergency, although the risk of gastric distension is great. The best method of removal is extraction under direct vision using a laryngoscope, forceps, suction or a finger.

Tracheal or bronchial foreign bodies produce persistent cough and wheeze, and recurrent pneumonia. A foreign body lodged in the upper oesophagus may compress the trachea and present with either acute or, more commonly, persistent stridor. Radiopaque materials are easily shown radiologically, but both anteroposterior and lateral views may be necessary. Barium studies may prove useful for non-radiopaque material in the oesophagus. Treatment is removal at bronchoscopy or oesophagoscopy.

ANTERIOR MEDIASTINAL TUMOURS

Anterior mediastinal tumours, such as lymphoma, may compress the trachea or bronchi, causing symptoms such as dry cough, stridor or wheeze. Airway compression may become severe enough to cause hyperinflation or atelectasis. Pleural effusions are common and may add to the respiratory distress. This is a high-risk situation. Symptoms may be aggravated by the supine position, especially during anaesthesia for a biopsy procedure. This is likely in patients with superior vena caval syndrome. Postural symptoms or findings on flow–volume loops may allude to this risk. Echocardiography may also provide evidence of cardiac compression which increases the risks associated with anaesthesia. Sudden complete obstruction that cannot be bypassed by a standard tracheal tube has been described. The use of armoured tubes or a rigid bronchoscope may be required. Consideration should be given to leaving the tracheal tube in situ postoperatively until corticosteroids and chemotherapy reduce the tumour mass.

ANAESTHESIA FOR RELIEF OF AIRWAY OBSTRUCTION

Inhalational induction and anaesthesia with oxygen and halothane or sevoflurane is the preferred technique for intubation. The use of muscle relaxants is hazardous if the ability to maintain a patent airway is doubtful.

Important points are:

• A prepared induction should be undertaken with efficient suction apparatus, a range of tracheal tubes, suitable stylets and bougies. Preparations must be made to intubate without deep anaesthesia if sudden obstruction occurs.
• Inhalational anaesthesia is slow in upper-airway obstruction, particularly when accompanied by lower airway or lung disease.
• Induction in the sitting position is advocated with epiglottitis. The child is laid flat after induction and prior to intubation.
• CPAP or assisted ventilation will reduce obstruction (minimise the dynamic component) and hasten induction. Care must be taken not to distend the stomach.
• Laryngoscopy is performed, and the child intubated, only when adequate depth of anaesthesia is achieved (e.g. approximately 8–10 minutes of 4% halothane in oxygen). Others recommend 6–8% sevoflurane.
• Orotracheal intubation is quickest and safest, and should be performed initially. After good tracheal toilet, the tube is changed to a nasotracheal one. Muscle relaxants may be used at this point if the operator is confident of the ability to intubate and/or ventilate.

CARE OF NASOTRACHEAL TUBE

Successful management of URTO in children requires optimal care of the nasotracheal tube. Such children must always be nursed in an ICU with adequate nursing ratios. The nasotracheal tube must be positioned at the level of the clavicular heads (T2) on an anteroposterior chest X-ray. Length of the tube from 1 to 6 years of age (in cm measured at the nose) is given by age in years + 13 cm. A meticulous technique of fixation must be employed to prevent accidental extubation.

Adequate humidification is difficult in the active child. Nevertheless, it is important to prevent obstruction of narrow tubes by inspissated secretions. Lightweight heat and moisture exchangers (HME) are very useful (e.g. Thermovent, Gibeck, and Humidvent, Portex). The HME should be changed every 24 hours to reduce contamination and increased resistance. Oxygen supplementation can be provided, if necessary. Some children will tolerate connection of a humidified T-piece.

Effective bagging and tracheal toilet is vital, and should be repeated until the airway is clear. Instillation of saline (0.5–1.0 ml) prior to suction may be necessary to remove secretions. Light sedation is used to improve tolerance of the tracheal tube and to reduce the risk of self-extubation. Midazolam, 0.1–0.2 mg/kg statim, followed by continuous infusion (0.05–0.2 mg/kg per hour) is effective. Arm restraints may also be advisable, particularly in very young children. In some restless young children, it may be safer to use heavy sedation and mechanical ventilation. Signs of obstruction are usually relieved by intubation. Mild retraction may persist in children with high fever and increased minute ventilation in the presence of a smaller than predicted tube. Fibreoptic bronchoscopy can be performed to confirm patency. The tracheal tube must be changed or removed if there is doubt about its patency.

Nasogastric tube feeding should be commenced in children who require intubation longer than 24 hours.

TRACHEOSTOMY

Tracheostomy remains a life-saving procedure and must be undertaken if tracheal intubation is impossible, or if appropriate equipment and personnel to facilitate intubation are unavailable. For chronic airway problems, it is more comfortable, allows better nasopharyngeal toilet and permits the child to leave the ICU and eventually return home. It is best performed under endotracheal anaesthesia with the neck extended. When intubation is impossible, the tracheostomy can be performed under anaesthesia via a laryngeal mask airway. A longitudinal slit is made through the second and third tracheal rings without removal of cartilage. Stay sutures in the tracheal wall lateral to the incision aid recannulation if accidental dislodgement occurs prior to formation of a well-defined tract (after 4 days). A postoperative chest X-ray should be obtained to check the position of the tip of the tracheostomy tube and to exclude pneumothorax or other complications.

Care of a newly created tracheostomy is similar to that of an endotracheal tube, with the additional problem of some discomfort and the likelihood of fresh blood in the airway. The first tracheostomy tube change is undertaken once a tract has been established, usually between 5 and 7 days.

CRICOTHYROTOMY

A wide-bore plastic i.v. cannula (14- or 16-gauge) passed into the trachea via the cricothyroid membrane may be life-saving if alternative procedures are unavailable. This should be performed with the neck extended as for tracheostomy. A system of connection to a low-pressure oxygen supply must be planned in advance. One method is to attach the hub of the cannula to the sleeve of a plastic 2–3 ml syringe (without plunger) to an adaptor from a 7.5 mm outer diameter tracheal tube, and then to a breathing circuit (e.g. Jackson Rees modification of Ayres T-piece). Jet ventilation has also been performed through a narrow cannula in this situation.

REFERENCES

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