NEONATAL UPPER AIRWAY OBSTRUCTION

DAVID ALBERT FRCS

INTRODUCTION

It is often a relatively inexperienced paediatric resident who is “first on the scene” when a neonate is delivered with upper airway obstruction. Sometimes simple measures such as suction are all that is required, moving on to a trial of an oral airway and finally intubation. Once stabilised these neonates can have the cause of their obstruction investigated in the cold light of day using the experience of other specialists and an array of highly technological investigative techniques. Just occasionally, intubation is either not possible, or does not relieve the obstruction, demanding a rapid response from whoever is available to help. Rarely, and very worryingly, even an emergency tracheostomy may fail to relieve the obstruction due to low tracheobronchial pathology. Airway obstruction may also occur after extubation of the intubated neonate or develop in the first few days or weeks of a neonate’s life.

It is important to realise that the likely causes of upper airway obstruction differ greatly in the different clinical situations outlined above. As a practical guide, this chapter will thus first cover the main clinical situations in which one is likely to meet neonatal upper airway obstruction, then the likely causes and the immediate management. It will then cover a general approach to diagnosis and management of obstruction, both above, and below the larynx. Finally, specific conditions will be listed providing a review of the causes of neonatal upper airway obstruction.

The structure of this chapter is thus:

Ø Clinical situations involving neonatal upper airway obstruction

w Antenatal diagnosis of High Airway Obstruction

w Unexpected airway obstruction at birth – nasopharyngeal

w Unexpected airway obstruction at birth – laryngeal

w Unexpected airway obstruction at birth - tracheobronchial

w Airway obstruction at extubation

w Airway obstruction developing shortly after birth

Ø General approach to diagnosis and management

Ø Specific Conditions

w Nasal

w Nasopharyngeal and Oral

w Laryngeal

w Tracheobronchial

CLINICAL SITUATIONS

Antenatal diagnosis of High Airway Obstruction

Routine prenatal ultrasonography looking for congenital anomalies should demonstrate large obstructing masses such as cervical teratoma^1,2, cystic hygroma³ and rhabdomyosarcoma⁴, the anatomy of which can be further defined using magnetic resonance imaging^5,6. Even in the absence of a mass, airway obstruction can be inferred, as with the tracheal dilatation and enlarged lungs seen in laryngeal atresia ^7,8. Polyhydramnios may occur with obstructing lesions, reflecting impaired fetal swallowing.

Forewarned should be forearmed, so that resources can be mobilized and management discussed before the child is born. Hollinger describes the successful airway management of a case in 1985¹ and Catalano reports a tracheotomy with intact maternal-fetal circulation, possibly the first such extrauterine surgical procedure⁵. Since then the term CHAOS has been used to describe antenatally diagnosed Congenital High Airway Obstruction.

The term “OOPS”, (Operation On Placental Support)³ has been replaced by the more acceptable EXIT procedure; Ex Utero Intra-partum Treatment^7-9. The multi-specialty team usually involves pediatricians, obstetricians, anesthetists and ENT surgeons with other specialities involved depending on the results of the ultrasound and MRI. At planned Caesarean section the airway can be established with expert intubation¹⁰ or occasionally a tracheostomy^7,8 is performed if intubation is not possible. Extra corporeal membranous oxygenation can be made available¹¹ but intubation or tracheostomy are faster and preferable. Resection of an obstructing mass is usually delayed until the child is stable¹¹.

Unexpected airway obstruction at birth – nasopharyngeal

In the absence of antenatal diagnosis, the unfortunate midwife, obstetrician or pediatrician is presented unexpectedly with a neonate with airway obstruction. Nasal suction to remove secretions is combined with an attempt to pass a nasal sucker. Choanal atresia is the commonest diagnosis in true nasal obstruction. Occasionally neonates referred with a diagnosis of choanal atresia on the basis of inability to pass a sucker have normal CT appearances. Presumably in these neonates the sucker’s passage is impeded by a tortuous route around the turbinates. Pyriform aperture stenosis, mid nasal stenosis and choanal stenosis are less common causes. These nasal causes of obstruction will be relieved by an oral airway as will nasopharyngeal masses such as nasopharyngeal teratomas.

Unexpected airway obstruction at birth – laryngeal

Airway obstruction relieved by intubation, but not an oral airway, implies obstruction at the laryngeal level. These include dynamic causes such as severe laryngomalacia and vocal cord palsy. Displaceable lesions such as laryngeal polyps and masses will also be relieved by intubation. In laryngeal stenosis it may be possible to force the tip of a small shouldered tube through the stenosis as a temporary measure to secure the airway. Some units now advocate using a laryngeal mask ¹² for neonatal resuscitation, which has the advantage that a tight stenosis will not be worsened by attempts at intubation. Very rarely, in laryngeal atresia with a low tracheo-oesophageal fistula, it may be possible to ventilate the neonate, though on closer examination the tube is actually in the oesophagus with ventilation via the fistula.

With low tracheal and bronchial obstruction, intubation is possible but does not relieve the problem.

When intubation is not possible, time is at a premium and the neonatologist is faced with a real challenge. If adequate ventilation is not possible with a laryngeal mask or very fine endotracheal tube, a decision has to be made to open into the trachea. Cricothyroid membrane or tracheal needle puncture may be the best option for a neonatolgist used to finding small arteries and veins but is not easy in an emergency situation without previous experience. The neonate needs to be straight with the neck extended over a roll. The first and second fingers of the left hand are placed either side of the trachea and the needle inserted vertically and very strictly in the midline until air can be aspirated. It is difficult to palpate cricoid and thyroid cartilages in a neonate and it is more important to remain midline rather than worry about the level. Further and larger needles can be inserted above or below the first. Open tracheostomy in an emergency is again difficult even for an experienced surgeon unless he has current experience of neonatal tracheostomy. The neonate again needs to be straight and with the neck extended. A long vertical but strictly midline incision with careful palpation of the trachea should avoid drifting off the midline, which is the main danger.

Laryngeal lesions such as congenital webs or subglottic stenosis will be bypassed with a tracheostomy but low lesions such as tracheal stenosis and tracheobronchial malacia will not.

Unexpected airway obstruction at birth - tracheobronchial

The risk with low tracheobronchial obstruction is that neither intubation nor tracheostomy will relieve the obstruction though positive pressure will tend to improve malacia and, to a lesser extent, stenosis. An extended (long) tracheostomy will physically support tracheomalacia but not carinal malacia or bronchomalacia. A most difficult situation occurs if a tracheostomy is attempted for tapering long segment tracheal stenosis. Not only is it is not possible to insert a normal neonatal size tracheostomy tube but the tracheostomy itself severely limits the therapeutic options for surgical reconstruction of the stenosis.

Airway obstruction at extubation

Post-extubation laryngeal edema can be predicted if there is no leak around an appropriate size tube. In these circumstances steroids can be given pre-extubation and CPAP and adrenaline nebulisers readied in case they are needed. Despite this some neonates will require re-intubation because of stridor, recession and airway compromise. It is often better to leave the neonate intubated for a while to avoid repeated attempts at extubation which merely compound the problem with further laryngeal damage. Graham¹³ has written on the concept of formal re-intubation which may be helpful by allowing the laryngeal mucosa to recover.

If extubation fails despite a period of “laryngeal rest” then an endoscopic examination is performed to diagnose the cause and to treat simple lesions endoscopically such as vocal cord granulations. These often wrap around the tube and once extubated look like “seal flippers”. Subglottic cysts are the other easily remediable cause and can be lasered or removed with careful forceps dissection. If there are no discrete lesions but merely a diffuse subglottic and glottic edema then consideration needs to be given to a cricoid split, a single stage laryngeal reconstruction or a tracheostomy (see below). Other causes such as a congenital laryngeal web or severe tracheobronchomalacia will usually require a tracheostomy initially before definitive treatment.

Airway obstruction developing shortly after birth

Laryngomalacia typically presents not with the first breath but over the first couple of days. Immediate stridor should alert one to the possibility of other causes such as vocal cord palsy or static lesions such as laryngeal web^14-16 cyst¹⁷ and stenosis^18-20.

Laryngomalacia^21-23 is the commonest cause of “congenital stridor” but it is by no means the only cause. Unfortunately the 2 terms are often used synonymously and a child is often labelled with “congenital stridor” as a diagnosis rather than a description. Other possible diagnoses such as vocal cord palsy, then tend to be ignored. Subglottic haemangioma^24-28 usually develops progressively in the first few months, later than most other neonatal causes of airway obstruction.

General approach to diagnosis and management

Diagnosis

History

When presented with a neonate who has failed extubation, the otolaryngologist needs to glean as much information as possible from the neonatologist to try to distinguish the possible causes for failed extubation. Key to this is the intubation history. Subglottic stenosis is not always associated with prolonged intubation^29,30 and an initial traumatic, emergency intubation may be more relevant. Shouldered tubes³¹ with the shoulder passed through the glottis can cause damage as can oversize tubes placed to improve ventilation or endotracheal tube patency³². Lack of an initial air leak around the tube or any tightness on intubation may suggest a narrow subglottis either associated with prematurity, Downs syndrome³³ or as part of the normal range³⁴.

In neonates that present with stridor at birth, the obstetric history is relevant as traumatic labour is responsible for 20% of vocal cord palsy³⁵. Stridor occurring immediately after delivery should always raise suspicions of a vocal cord palsy. Any diurnal or other variation can help identify the cause with laryngomalacia typically being better with the child at rest and asleep but made worse by crying, feeding and when distressed. Airway obstruction with the baby supine can occur with a pedunculated laryngeal mass but more often is due at least in part to a degree of supralaryngeal obstruction such as micrognathia and resultant tongue base occlusion. Improvement in the airway with crying occurs in gross nasal obstruction such as bilateral choanal atresia.

It is important to ask about symptoms other than stridor. These include apnoeas, cyanosis, a hoarse cry and feeding difficulties. Apnoeas with cyanosis are typical of severe tracheobronchomalacia and are sometimes termed “dying spells”. Hoarseness clearly suggests a laryngeal lesion such as a laryngeal web or vocal cord palsy.

Feeding is closely connected with breathing particularly in the neonate and an accurate picture of the feeding pattern must be obtained. Aspiration suggests a vocal cord palsy, tracheo-esophageal fistula or rarely a cleft larynx with recurrent chest infections usually accompanying significant aspiration. Regurgitation is common in neonates and by itself may not represent significant gastro-esophageal reflux. The end result of poor feeding may just be slow troubled feeding which troubles the mother more than the child or may result in failure to thrive with demonstrably poor weight gain.

General medical inquiry may explain a vocal cord palsy occurring as a result of neurological disease or cardiac surgery or may suggest vascular compression associated with congenital cardiac disease. Finally ask the parents about the presence of any birthmarks, as they may be associated with a subglottic haemangioma.

Examination

Typically, inspiratory stridor is due to an extrathorasic obstruction in the larynx or high trachea with bronchial obstruction producing an expiratory stridor (Fig 1). Biphasic stridor can occur with obstruction anywhere in the tracheo-bronchial tree. Expiratory stridor may be absent but a prolonged expiratory phase may be present indicating an intrathorasic obstruction (Fig 2). The characteristic sound of stridor, even in a common condition such as laryngomalacia, is so variable as to be of little diagnostic use on its own. Laryngomalacia is said to have a ‘musical quality’, vocal cord palsy a ‘breathy quality’ and the cough in tracheomalacia to be ‘barking’. The site of the abnormal vibration can rarely be tracked down with the aid of a stethoscope because of the variable transmission of sound through the thorax. Auscultation is however useful to detect heart murmurs and wheeze.

Subcostal, intercostal and suprasternal recession may occur separately or together and also be associated with see-saw respiration. The severity of recession is a better indicator of the severity of airway compromise than the degree of stridor which can paradoxically become less obvious as obstruction worsens due to the diminishing airflow.

If a supralaryngeal component is suspected nasal patency should be assessed with a mirror, a wisp of cotton wool or using the bell end of a stethoscope and a conscious assessment made of jaw and tongue size.

Both stridor and recession will vary as the child rests, cries and sleeps but it is rare to able to demonstrate a similar repeatable change with position. Observing the child feeding is very valuable particularly if poor feeding or aspiration are significant features in the history.

Imaging

The most appropriate imaging technique will depend on the suspected site of neonatal airway obstruction. For nasal lesions, a CT scan identifies abnormalities such as choanal atresia³⁶, choanal stenosis³⁷, vestibular stenosis^38,39 and pyriform aperture stenosis^40-43. It is important that the nasal cavity is sucked clear of secretions first to avoid a spurious diagnosis of membranous choanal atresia⁴⁴. Magnetic resonance imaging should also be employed to demonstrate possible intracranial connections in suspected encephalocele, meningocoele and nasal glioma^45,46 as CT alone can be misleading. 3D reconstructions of the cranial CT’s are used to in plan craniofacial reconstructions and give a clear appreciation of the midface and mandibular deficiency that predisposes to airway compromise (Fig 3). In the pharynx, an MRI is particularly useful for vascular lesions such as haemangioma and lymphangioma. Lesions within the laryngotracheobronchial tree such as stenosis are sometimes visible on a plain chest x-ray or a penetrated filtered (Cinicinnati) view. The current resolution of CT and MRI scans^47-49 does not usually give sufficiently high definition to fully characterize a stenotic segment⁵⁰, even if software is used to reconstruct the image three-dimensionally. For extrinsic lesions, particularly vascular compression, an MRI is however the investigation of choice. Videofluoroscopy is an excellent way of demonstrating tracheomalacia and can be combined with a contrast swallow looking for vascular compression^51,52 and aspiration. Bronchography is now much safer with the introduction of non-ionic contrast media. It is particularly useful for the lower airway demonstrating tracheobronchial stenosis and malacia. Echocardiography can be used to screen for vascular compression demonstrating most but not all abnormal vasculature as well as coincidental or symptomatic congenital heart disease.

Gastro-esophageal reflux is very common in neonates and may also be the result rather than the cause of airway obstruction with negative intra-thoracic pressures. The role of pH studies is therefore rather limited unless more complex studies measuring upper esophageal or pharyngeal pH are available⁵³.

With experience, ultrasound of vocal cords can be used to demonstrate vocal cord palsy with reasonable accuracy to complement the endoscopic findings. Transcutaneous electromyography is helpful in the adult situation especially if the nerve has been severed. In the pediatric situation the nerve is usually intact and action potentials can be identified even in the presence of an established bilateral cord palsy. Technical problems have limited the use of EMG in children even under the controlled conditions of anaesthetized endoscopy.

Endoscopy

Neonatal airway endoscopy has to be safe as well as providing accurate diagnostic information. To achieve these objectives requires not only a full range of specialized paediatric endoscopy equipment but, most significantly, a high level of experience in the endoscopist, anesthesiologist and nursing staff. Too often a unit will perform an inadequate evaluation which will only need to be repeated. If in doubt refer to a center with sufficient experience to perform a single comprehensive and definitive evaluation. A systematic approach will provide a diagnosis in most cases.

Awake flexible laryngoscopy⁵⁴ has the advantage over conventional rigid endoscopy under anaesthesia of interfering less with dynamic conditions. The introduction of ultra-thin endoscopes^55-57 with good optics and a diameter of less than 2mm has allowed even neonates to be endoscoped without the need for a general anaesthetic. Awake endoscopy is less controlled than under anaesthesia but in selected cases is safe with an experienced endoscopist. Laryngomalacia can usually be distinguished from vocal cord palsy but if the collapse from laryngomalacia is severe it is sometimes not possible to visualise the glottis and therefore exclude a co-existing cord palsy. Lesions below the glottis are not well visualised which raises the issue of co-existing lesions which can be as frequent as 5%. It should therefore be viewed as a screening procedure

Rigid laryngotracheobronchoscopy under general anesthesia is still the investigation of choice for all complex airway lesions. It is a highly technical procedure and the whole team (surgeon, anesthetist and nursing assistant) need to fully understand the equipment to perform the examination safely; and to optimize the assessment. Ideally the same surgeon, anesthetist and nurse should routinely work together and be used to dealing with neonates. Most units now use spontaneous ventilation as this is not only safer but also allows a dynamic assessment of the airway. Spontaneous ventilation is facilitated by topical anesthesia of the larynx and trachea. This prevents coughing without needing a level of anesthesia that prevents spontaneous breathing. Lignocaine dose needs to be carefully measured as the preparations used in adults can easily result in overdosage^58,59. Ideally intubation is avoided as this allows the larynx to be examined without any intubation artefacts. In the already intubated neonate being examined for failed extubation, it is often helpful to apply some topical adrenaline to the glottis around the tube so that when the tube comes out there is a better airway and thus more time for a careful examination.

The larynx is examined first with a microscope or rigid endoscope checking for cysts, webs and a posterior laryngeal cleft. The arytenoid movement is checked passively with a probe as cricoarytenoid fixation can mimic a vocal cord palsy. The time available for the examination will depend on the airway. In a child breathing spontaneously with a normal airway and normal lung function, anesthesia can be maintained solely by the use of inhalational agents with the endotracheal tube withdrawn into the pharynx. In others the time may be very limited and it is essential to be prepared to move ahead with a rigid ventilating bronchoscope at any stage. If there is significant subglottic stenosis an ultra fine telescope passed through the laryngoscope will cause less trauma than a bronchoscope.

The trachea and bronchi are examined next using an appropriate size bronchoscope is used unless stenosis is suspected (Fig 4). Neonates pose particular problems if manipulation of the airway is required^60,61. The main bronchi, the carina, the trachea and the subglottis are all systematically examined and videographs or digital images recorded. Tracheomalacia should be observed with a small bronchoscope withdrawn from the area in question and without positive airways pressure to avoid splinting. The ratio of cartilage to trachealis is significant in determining the type of malacia and if aortopexy is likely to be successful.

Dynamic assessment of the larynx on recovery from anesthesia aims to demonstrate the vocal cord movement and any supralaryngeal collapse (laryngomalacia). Typically this can be achieved by withdrawing the bronchoscope to just posterior to the tip of the epiglottis. This affords a good view of the vocal cords to exclude a cord palsy and of the arytenoids to exclude the common posterior form of laryngomalacia, though anterior collapse of the epiglottis may be masked. In this case a 30° or 70° telescope should be used. The anesthetist should call the phase of respiration to check for paradoxical vocal cord movements caused by the cords being sucked in passively on inspiration by the negative airways pressure created by the air flow. With active cord movement the cords abduct (move apart) on inspiration due to the action of the posterior cricoarytenoid muscle.

Videographs of the examination allow a meaningful discussion between otolaryngologist and neonatologist with a permanent record for comparison in the future.

Treatment

Nasopharyngeal airway obstruction can be improved medically with saline, suction and topical steroids, though the dose and duration of topical steroids in neonates needs to be carefully monitored. Vasoconstrictor nose drops such as 0.5% ephidrine also need to be used with care. Nasal airways can either be purpose-made prongs or a shortened endotracheal tube with the end sitting in the nasopharynx or oropharynx. Such airways act as stents maintaining an airway through a narrow edematous nasal cavity or posteriorly placed palate or tongue base. Surgical options in the nose include endoscopic choanal surgery to address choanal atresia, and open operations such as lateral rhinotomy and external rhinoplasty to remove nasal masses such as nasal gliomas.

Laryngeal airway obstruction can sometimes be bypassed with intubation but otherwise will usually require endoscopic or open laryngeal surgery. These techniques are used as initial treatment to avoid tracheostomy if possible. Endoscopic treatment of the neonatal larynx requires considerable experience of both surgeon and anaesthetist as well as specialized equipment. Aside from the immediate risk of dealing with an unstable neonatal airway any damage to the delicate vocal fold can produce dysphonia that will remain for a lifetime and prove difficult to correct. Endoscopic procedures commonly used in neonates include resection of small subglottic cysts and removal of cord granulomas. The CO₂ laser can vaporize small lesions without bleeding but must be used carefully in the subglottis to avoid stenosis. Aryepiglottic trimming for larygomalacia removes a small wedge of the aryepiglottic mucosa on each side to prevent the forward prolapse of the posterior larynx and arytenoids which is typical of the condition. Open surgery on the neonatal larynx is usually for developing subglottic stenosis and consists of a cricoid split or immediate laryngeal reconstruction using rib cartilage. Surgery is followed by a period of elective intubation prior to planned extubation under steroid cover.

Tracheostomy is used to bypass laryngeal or tracheal obstruction that can not be dealt with by endoscopic or open surgery. It is also used if the child will require long term ventilation or to support physically an area of tracheomalacia. Neonatal tracheostomy has particular risks because of the small dimensions. The tube is more likely to block than in an older child and is also more likely to become displaced. There is a narrow margin between the tube tip being past the carina and tending to come out of the stoma. Tracheostomy is usually conducted intubated and under general anesthesia with the child supine. Rigorous haemostasis is ensured with microbipolar diathermy forceps (Fig 5). A vertical incision is made through the 3rd and 4th tracheal rings with stay sutures placed either side of the incision (Fig 6). The correct tube length should be checked on the operating table by listening to the right lung with the head flexed. It is important to use a large enough tube to allow ventilation without a significant leak past the tube. A fairly tight fit of the tracheostomy tube into the trachea also minimizes air escape and facilitates ventilation. Any skin sutures should not close the wound too tightly to prevent subcutaneous emphysema but a very open wound as used in adults does not heal well in neonates. Post operatively a chest x-ray will check the tube length and exclude a rare pneumothorax which can occur from puncturing the lung apex or in neonates from high pressure ventilation. Tube dislodgment and blockage remain the most important late complications and are responsible for the mortality of 1-2%. There is now a move to avoid neonatal tracheostomy, with tracheostomy now only being used after a failure of initial surgery.

Specific Conditions

Nasal conditions

Neonates are obligate or at least preferential nasal breathers and will become cyanosed rather than open their mouth to breathe.

Neonatal rhinitis is a common condition with nasal obstruction from increased secretions and mucosal edema⁶². It is usually due to allergy or non specific infection although occasionally a swab will show a specific infection such as Chlamydia ⁶³.

The nasal dimensions are smaller than normal in choanal stenosis, choanal atresia, mid nasal stenosis and vestibular stenosis⁶⁴. The site and extent of narrowing can be estimated by passing a catheter or assessed accurately with a CT scan. Choanal atresia can be unilateral or bilateral and isolated or associated with other congenital abnormalities such as in CHARGE syndrome⁶⁵. CHARGE stands for: C-coloboma of the iris and retina, H-heart disease, A-atresia choanae, R-retarded growth, G-genital hypoplasia, E-ear defects.

Nasal tumours include gliomas, nasal dermoids, encephalocoeles, meningocoeles, lipomas, fibromas and nasolacrimal duct cysts⁶⁶. Treatment is surgical once an intracranial connection has been excluded radiologically⁴⁵. Haemangiomas can be observed but may eventually need plastic surgery if resolution is not complete.

Nasopharyngeal and Oral conditions

The physical size of a large tongue, macroglossia, or a small mouth, microstomia, can cause oropharyngeal airway obstruction alongside the tongue retrusion seen with micrognathia and the poor nasopharyngeal airway in maxillary hypoplasia. The common craniofacial syndromes causing obstruction include Pierre Robin^67-71, hemifacial microsomia and Crouzons. The hairy polyp or nasopharyngeal teratoma derives from two germinal layers, ectoderm and mesoderm⁷² and requires simple surgical excision^73-75.

Laryngeal conditions

Laryngomalacia^21-23 is most commonly due to the forward prolapse of the posterior supraglottic structures; the arytenoid cartilages and the aryepiglottic folds. Anatomically the aryepiglottic fold is found to be shorter, tending to pull the arytenoids forward to the tongue base. The supraglottic collapse on inspiration increases with increasingly negative negative airways pressures from increased airflow. The stridor is therefore worse on crying and feeding but tends to be better when the child at rest. If it is associated with severe failure to thrive the short aryepiglottic fold can be divided^21,76-81.

Vocal cord palsy is the second most common cause of neonatal stridor, accounting for 10% of all congenital laryngeal anomalies^82,83. It presents within the first month of life with stridor, cyanosis, apneas and feeding difficulties. Flexible fibreoptic endoscopy is a good initial investigation. It should be followed by rigid endoscopy to allow manual palpation of the cords, to distinguish true paralysis from cricoarytenoid joint fixation⁸⁴. Laryngeal ultrasound is improving with better scanners, smaller probe sizes and more experience⁸⁵. Many neonates, especially those with unilateral cord palsy, will cope without intubation or a tracheostomy. Reported tracheotomy rates vary from 0 to 36% for unilateral VCP^35,86 and 0 to 73% for bilateral cases^35,87. In the absence of an obvious cause such as birth trauma or cardiac surgery a neurological opinion should be sought to exclude hydrocephalus, congenital hypotonia, Mobius syndrome, cerebral palsy, arthrogryposis multiplex congenita, leukodystrophy, hypoxic encephalopathy and Charcot-Marie-Tooth disease. Spontaneous recovery does occur being more likely in unilateral cases (70%) then bilateral (80%)^84,86.

Congenital subglottic stenosis is due to a thickened elliptical cricoid cartilage⁸⁸ occasionally with a trapped first tracheal ring. The stenosis can be truly subglottic or involve the vocal cords as in a congenital laryngeal web, which almost always has a significant anterior subglottic component⁸⁹. The stridor and recession in a significant stenosis may be quite unremarkable if airflow is reduced. This is a trap for the unwary, as any attempt at intubation can cause edema and rapid airway obstruction.

Acquired subglottic stenosis from neonatal intubation (Fig 7) is treated conservatively at first with steroids and a planned extubation after a period of laryngeal rest¹³. Minor lesions such as granulations and cysts are then excluded(Fig 8). Developing soft stenosis(Fig 9) can be relieved with a cricoid split. The split is achieved via an external incision and opens the larynx anteriorly from just beneath the vocal cords to the first tracheal rings. The gap produced in the cricoid is not great and it may be that the operation owes its success to decompression as much as releasing the integrity of the cricoid ring. The neonate is intubated for 2-5 days after which extubation is successful in 70%^90-93. If the stenosis is found to be firm at endoscopy, augmentation is required with costal cartilage. This can be achieved in the neonate with an immediate laryngeal reconstruction(Fig 10) leaving the neonate intubated at the end of the procedure. The complication rate of immediate reconstruction in neonates is higher than in single stage laryngeal reconstruction in older children⁹⁴ but it may avoid tracheostomy, which also has a higher complication rate in neonates. In complex neonates with poor cardio-respiratory function or multiple congenital anomalies a tracheostomy and laryngeal reconstruction after an interval is preferable^95-100 as in childern with established severe stenosis (Fig 11).

Tracheobronchial

Tracheal stenosis can be isolated or affect the whole length of the trachea often with abnormal or complete tracheal rings. Both tracheostomy and intubation should be avoided if possible and the neonate transferred to a centre with experience of these complex and difficult anomalies. Surgical options include grafting with pericardium or cartilage as well as resection or tracheoplasty. Postoperative stenosis or collapse can be supported with endoscopically placed expanding metal stents which are dilated with an endoscopic balloon^101-103.

Tracheomalacia¹⁰⁴ is an abnormal collapse of the trachea which when severe can produce symptoms of airway obstruction with expiratory stridor, cough and cyanotic attacks. Unexplained respiratory distress on the neonatal intensive care unit^105,106 may be due to tracheomalacia and with the myriad of other possible causes can often be missed. Primary or intrinsic malacia^105,107 is due to an abnormality in the wall of the airway; secondary malacia is due to extrinsic compression, often vascular. An aberrant innominate artery compresses the right anterior trachea just above the carina. A double aortic arch surrounds the trachea and main bronchi producing concentric or triangular shaped compression at endoscopy. A pulmonary artery sling compresses the right main bronchus often to the extent that the lumen of the right. Vascular anomalies are demonstrated on echocardiograph and MRI⁴⁷. Mild primary tracheomalacia usually requires no treatment as the disease is self-limiting over 1-2 years and resolves without surgery¹⁰⁸. Aortopexy was initially used in tracheomalacia associated with tracheoesophageal fistula^109,110 but has also been used primary tracheomalacia^105,107. An extended tracheostomy tube¹¹¹ will effectively support midtracheal tracheomalacia but is less effective for low tracheal and bronchial collapse.

Brochomalacia is the equivalent collapse in the bronchi. Occasionally bronchomalacia can be improved with a suspension procedure¹¹²though this is less established than aortopexy. Carinal tracheomalacia and severe bronchomalacia can be supported with Continuous Positive Airways Pressure (CPAP)^113,114 from a standard home CPAP machine as used in obstructive sleep apnoea. The device can be used nasally with a close fitting mask (with some difficulties of acceptance) or via a tracheostomy tube. Internal stents support the area of collapse well but suffer from migration, extrusion and localized reactions including granulations and frank infections. Both siliconized plastic and expandable metal stents have been used with success. The expandable metal stents^102,115-117 are difficult to insert even using an introducer and need to expand at just the right point in the lumen once released. Balloon dilatation can be used to further increase the lumen to accommodate future growth¹¹⁷.

Summary

Neonatal airway obstruction, especially if unexpected, can prove a challenge for all concerned. An appreciation of the rarer causes can help avoid some of the pitfalls such as trying to establish in a tracheostomy in a child with a long segment tracheal stenosis. Forward planning for neonatal units, with protocols for managing common situations such as failed extubation, should improve outcomes and ensure that the appropriate specialist is involved at an early stage.

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