There are many conditions of the upper and lower airways that may require medical and surgical intervention or otherwise would have an adverse effect on pulmonary status.  In the neonate these problems can be categorized as either congenital or acquired, though the distinction sometimes becomes blurred.  These can then be classified as extra or intrathoracic and further as to whether the obstruction is due to anatomical or pathophysiological abnormalities of the airways.  This regional / etiological framework is designed only to assist in the creation of a structured differential diagnosis scheme and facilitate a more rapid diagnosis, and subsequent appropriate management whether medical or surgical.

LOCALIZATION OF STRIDOR

Snorting respiratory sounds from the neonate in distress tend to be associated with nasal or nasopharyngeal obstruction.  Inspiratory stridor (or abnormal inspiratory breathing sounds) usually localize the lesion to the supraglottis, while expiratory stridor places the problem in the subglottis.  To and fro stridor tends to originate from the vocal cords or from immediate subglottic disease.  A barky cough can localize a lesion to the vocal cord or subglottic region, while a brassy cough can suggest a distal tracheal or bronchial intrathoracic lesion1.

ETIOLOGY

CONGENITAL 

Congenital extrathoracic anatomic malformations that result in airway obstruction in neonates include lesions in the nose, nasopharynx, oropharynx, oral cavity, hypopharynx, larynx, and the proximal trachea.  The spectrum of nasal abnormalities includes, lacrimal cysts, nasal stenosis, agenesis of the nose, as in the cyclops malformation, masses, and choanal atresia2,3.  The masses can be tumors such as rhabdomyosarcoma, esthesio-neuroblastoma or encephaloceles4,5.  The encephalocele presents as a gray fleshy mass sometimes indistinguishable from the nasal turbinates, but represents brain tissue that usually is connected to the rest of the brain by a stalk through an aperture in the cribriform plate6,7.  The MRI scan has provided the best means of establishing the presence of an encephalocele8.    The brain signal lights up in contrast to the adjacent nasal tissue.  The greatest risk of these lesions is of meningitis9,10.  Another more common cause of nasal obstruction is choanal atresia (occurrence one in 8000 births), which is a failure of the posterior nasal aperture to open; and can be  either membranous or bony in nature11.  Both the nasopharynx and the orophayrnx can be obstructed by an epignathic teratoma (an aborted embryologic remnant attached to the base of the skull).  The oral cavity lesions include cavernous syndromes such as the continuous spectrum of cystic hygromas (purely lymphoid), lymphangiomas (mixed), and hemangiomas (purely vascular).  These are detectable prenatatally by ultrasound in many cases.  In Crouzons and Aperts syndromes the midface can encroach on the nasopharynx producing obstruction12.

The Pierre Robin anomaly, which is relatively rare (occurrence of one in 30,000 births), consists of mandibular hypoplasia, glossoptosis and a midline posterior cleft of the palate13,14.  It produces obstruction by the apposition of the tongue against the posterior pharyngeal wall; and is accentuated by the surface tension of the adjacent mucus membranes.  Laryngomalacia, Latin for soft larynx, is a collapsing lesion of the supraglottis, and is the most common cause of stridor in infants.  It can be either a floppy epiglottis that is sucked down over the laryngeal orifice by the venturi effect of air flowing over it during inspiration, or a tubular (omega, or soda straw) shaped epiglottis, or one foreshortened by attenuated aryepiglottic folds tethering the epiglottis down upon the larynx15.  Clinically it is characterized by a fluttering inspiratory stridor, that improves when the infant is placed prone.  Congenital laryngeal webs represent varying degrees of an embryological failure of the true vocal cords to completely separate.  Failure to cleave apart in utero can produce a fatal outcome in the delivery room from anoxia.  The stridor is to and fro, or absent if too little air is flowing16.  Congenital subglottic, is a failure of the upper laryngotracheal airway primordium to hollow out during the embryologic remodeling phase, and can be life threatening if severe17.  Subglottic hemangiomas can be congenital but more often become symptomatic and obstructive after a few months. 

Congenital extrathoracic pathophysiologic lesions occur in neonates with congenital disorders affecting innervation of skeletal muscles, with congenital myopathy, or birth injury to the spinal cord or peripheral nerves supplying the muscles of respiration, and are at risk for respiratory insufficiency after birth.  Congenital anterior horn cell disease and congenital myopathies present both acute and long term airway management problems.  The baseline resting muscle tone that supports the upper airway may be deficient and the infant may obstruct.  Central hypoventilation and Ondine's Curse patients are now routinely identified by pneumograms18.  Intranasal masses can be tumors such as gliomas, and astrocytomas.  Both the nasopharynx and the oropharynx can be obstructed by an epignathic teratoma (an aborted twin remnant attached to the skull base).  Not only can the airway be obstructed but it can also be permanently distorted by these living tissue masses.  Other oral cavity lesions include cavernous obstructive syndromes such as the continuous spectrum of cystic hygromas (purely lymphatic), lymphangiomas(mixed ), and hemangiomas (purely hemangiomatous).  These are now detectable prenatatal by ultrasound in many cases19,20,21.  Microstomia, in association with other minor anomalies, can produce obstruction as well.  Lingual thyroid tissue has even been reported as a cause of neonatal airway distress22.  Pyogenic granulomas resulting from mucosal injury during vigorous intubation of the meconium stained larynx can produce obstructing lesions within days.  Congenital laryngeal cysts, laryngoceles, and ventral laryngeal clefts can be obstructive as well23,24,25.  Subglottic hemangiomas usually present later in infancy but can be present at birth and obstruct.  Congenital goiter has also produced tracheal compression.  Vocal cord paralysis can be either congenital or acquired26,27,28.  The congenital form may result from a nuclear agenesis syndrome such as the Mobius syndrome29.  Vocal cord paralysis may be idiopathic, an isolated consequence of a traumatic delivery, or it may be associated with central nervous system defects such as myelodysplasis and Arnold-Chiari malformation30.  Hypoxia has been implicated in some infants with vocal cord paralysis, through documented fetal distress and subsequent lucencies in the region of the vagal nuclei of the brainstem on MRI .  In a traumatic delivery, the injury can be either subdural hematomas or a recurrent laryngeal nerve variant of Erbs' palsy31,32.  Post-traumatic vocal cord paralysis may be short in duration and require only close medical observation until resolution occurs; especially if the cords rest in a paramedian position.  Aspiration can be a problem through open or insensate vocal cords and lead to significant apnea, and pneumonia, particularly if it is central in origin.

Congenital intrathoracic anatomic malformations resulting in airway obstruction in neonates include lesions in the distal trachea and bronchi.  Vascular rings trap the trachea between two or more large vessels or ligmentous bands, such as double aortic arches and its many variants33,34.  Correction may not improve the trachealmalacic component though and obstruction can persist.  Foregut cysts can be extremely difficult causes of airway obstruction to diagnose in the neonate35 Tracheal stenosis is frequently associated with esophageal atresia and tracheoesophageal fistula.  Complete ring syndrome is a rare type of tracheal stenosis.  It is deformity where the usually horseshoe shapes of the tracheal cartilages are replaced by completely circular or spiral cartilages, resulting in a 80-90% reduction of the normal tracheal lumen diameter.  An early tip off to the presence of the complete ring syndrome is its frequent association with pulmonary artery sling.  Tracheal agenesis as dramatic as it can be can be compatible with life if there is an associated TEF36.  Tracheomalacia, is another collapsing lesion where the anterior tracheal wall lacks satisfactory rigidity to withstand the mild normal expansile pressure from the lung, heart and mediastinal tissues during inspiration37.  Duplication cysts usually produce obstruction later in infancy, but the redundant extra trachea, or esophagus or combination of the two can produce fatal compressive obstruction early.  Gastroesophageal reflux can produce respiratory obstruction in the neonate by causing a reflex laryngospasm, sometimes only detected by its associated bradycardia.

CONGENITAL OR ACQUIRED

Vocal cord paralysis can be either congenital or acquired or indistinguishable.  The congenital form may result from nuclear agenisis, such as the Mobius Syndrome, or intrauterine infection29,39.  Vocal cord paralysis may be idiopathic, an isolated consequence of a traumatic delivery, or it may be associated with central nervous system defects such as myelodysplasis and the Arnold-Chiari malformation30.  Fetal distress with hypoxia has been implicated in some infants with vocal cord paralysis.  Lucencies on MRI in the vagal nuclei region brainstem have been seen in some of those with central paralysis or paresis.  In a traumatic delivery the injury can not only be from hypoxemia but also from subdural hematomas or an Erbs' palsy type of stress to the recurrent laryngeal nerve.

ACQUIRED AIRWAYS OBSTRUCTION

Acquired airway obstructive problems also may also be separated into extrathoracic and intrathoracic.  Extrathoracic problems include infections acquired  both from the birth canal and hospital.  Nasal airway obstruction can arise from a fractured and displaced nasal septum as a result of difficult vaginal delivery.  Intranasal burns with synechia formation as a result of nasal prong humidifier malfunction.  Probably the most common type of acquired injury to the neonatal airway resulting in obstruction is due to post-intubation injury.  This can take the form of vocal cord paralysis, laryngeal stenosis / web formation, cysts, scar fixation of a vocal cord, subglottic edema and stenosis, or upper tracheal stenosis, malacia, or cyst formation.  Of all of these lesions post intubation subglottic edema followed by stenosis is the most common anomaly38.  Acquired laryngeal webs are bands of scar that bridge from one side of the airway to the other as a result of intubation with an endotracheal tube.

Intrathoracic problems include lower tracheal injury due to intubation, such as life threatening granulation tissue formation at the corina, and life threatening bradycardia from endotracheal tube pressure on the corina.  Injury can be secondary to compression of the lower airway from dilatation of the great vessels and heart chambers that sometimes is found in deteriorating complex congenital heart disease.

In phrenic nerve palsy, usually due to an injury to the cervical plexus sustained during birth, the pediatrician is alerted to possible diaphragmatic paralysis when the injury is associated with the typical weakness of the hand and forearm on the affected side (i.e., Erb's palsy).  However, in some cases the phrenic nerve paralysis may occur alone or after cardiovascular procedures.  In this instance there may be no external clues, except for a history in some infants of a "difficult" vaginal delivery, or failure to wean off the respirator.  Usually the injury to the phrenic nerve is unilateral and temporary.  The infant, while manifesting tachypnea, has little other evidence of respiratory failure.  These infants, however, require special surveillance, since they will have reduced ventilatory function and reduced tolerance to respiratory tract infections.  Follow-up evaluation should include monthly assessment of blood gases to monitor respiratory function and the use of real-time ultrasound study every two to three months to assess diaphragmatic function.  Return of diaphragmatic function,  if it occurs, may take three to six months.  With long-term paralysis, eventration of the diaphragm may appear.    

Injury to the recurrent nerve has been reported from placement of ECMO cannulas repair of TEFs, and placement of CVP lines.  Post-traumatic vocal cord paralysis may be short in duration and require only close medical observation until resolution occurs, especially is the cords rest in a paramedian position.  Aspiration can be a problem and lead to significant apnea, and pneumonia.  Many recover within one year.  In the Arnold-Chiari malformation the vocal cord paresis or paralysis may have a delayed onset and may be associated with the progression of hydrocephalus, or brainstem impingement.

PATHOPHYSIOLOGIC CONSEQUENCES OF OBSTRUCTION

IMPAIRED VENTILATION

The net physiologic impact of tracheal obstruction is impairment of ventilation.  Severe uniform hyperinflation may be the major clinical and radiologic finding.  More commonly, however, over distended lung segments coexist with atelectatic or partially atelectatic segments.  Blood gas abnormalities occur whenever the efficiency of gas exchange is diminished.  Acute respiratory acidosis is gradually compensated in long-standing upper airway obstruction by renal bicarbonate retention.  Less frequently, chronic hypoxemia results from upper airway obstruction.

MUCOUS MEMBRANE INJURY AND BRONCHOSPASM

Mucous membrane injury at the site of upper airway obstruction may complicate and worsen the pre-existing airways obstruction by causing delayed clearance of airways obstruction by causing delayed clearance of airways secretions, leading to pooling of mucus and formation of plugs of mucus.  Long-standing interruption in the mucociliary blanket and defective mucus clearance may result in increased bronchial reactivity, chronic bronchospasm, and permanent impairment of clearance mechanisms, as well as chronic or recurrent airways infection.

The initial event leading to impaired clearance probably is the alteration of mucociliary blanket function.  The mucociliary blanket is a protective barrier of the airways lining, as well as a primary mechanism for movement of mucus from the peripheral to the proximal airways for interferes with normal mucus flow and the airways cleansing function of the mucociliary blanket.  When this flow is interrupted, mucus-producing cells and glands hypertrophy, increasing production of substantially more viscous mucus.  Pooling of mucus increases the degree of obstruction.  This leads to either aseptic or bacterial inflammation of the airway.  Sloughing of the mucociliary blanket also may occur.  Submucosal tissues and the associated irritant nerve fibers may be exposed to potentially sensitizing agents in the stagnant mucus, resulting in increased bronchomotor tone and further reduction in airways caliber.  The chronic reflux of stomach content and laryngospasm or occasional aspiration pneumonia and bronchospasm must be dealt with

INFECTION

Persistence airway obstruction allows organisms in the mucus to overgrow and cause chronic airways infection, resulting in further mucociliary injury and dysfunction.  This produces an abnormal quantity and quality of mucus, which aggravates the pre-existing obstructive process.  Bronchial hyperactivity may worsen with each new episode of infection-injury.  Infection and injury at the alveolar level may lead to injury of the interstitium of the lung and eventual pulmonary fibrosis.  Nasal obstruction can occur in the neonate as a result of TORCH infections 39

MANAGEMENT 

DIAGNOSTIC IMAGING

Modern imaging technology can help evaluate and clarify the  cause of the neonatal airway distress.  If the child is stable and time allows one or several of these techniques can be utilized.  MRI defines the soft tissue aspects of cranial or neck lesions, while the CT scan shows air contrasts and solid structures of the nasopharynx and cartilage better40,41.  Arteriograms must play a role in the evaluation of vascular lesions, as do barium studies of the upper pharynx, esophagus, stomach for the aerodigestive tract.

MEDICAL METHODS OF TREATMENT

The medical management of an upper airway obstructive disorder is predominantly supportive.  While medical management is an important adjunct to the surgical management, in the absence of specific surgical repair options it holds the only promise for achieving and maintaining airway patency and thus preserving adequate acute or chronic ventilation in many cases 

ADMINISTRATION OF ANTIBIOTICS, ANTIFUNGALS AND ANTIVIRALS

The initiation of antimicrobials early in the course of a possible infection may be the turning point in the outcome of the infected neonate.  Caution must be stressed to avoid a shotgun approach to treatment; but rather a more selective process of evaluation is urged based on the probably that the condition is due to an infection or complicated by one.  Hospital acquired pneumonia are not infrequent in infant with compromised airways and subsequent compromised secretion clearance42.

ADMINISTRATION OF HUMIDIFIED GAS

The first objective of therapy is the prevention or relief of abnormalities in gas exchange.  Oxygen is also administered if the arterial oxygen partial pressure falls below 65 torr, or O2 saturation falls below 90%.  In some restrictive lesions rare gas mixtures of Helium and Oxygen have assisted in the maintenance of ventilation.    Warmed, humidified air is occasionally administered for inflammatory conditions of the trachea.  Life threatening mucus plugs have occurred from humidifiers that have run dry.  Nasal and upper respiratory tract burns as well as harden obstructive mucus plugs have occurred from heater-humidifier malfunctions, and thus these devises should be monitored as closely as the ventilators they support.

POSITIONING

Some young infants benefit from being placed, especially during sleep, in either the Fowler or prone position or occasionally supine with a "roll" under the shoulders.  This maximizes airway caliber and promotes efficient air flow.  Cadaver studies have demonstrated that the tip of an endotracheal tube can travel some distance in the trachea solely as a result of head positioning.  Neck extension pulls the tube up and away from the corina while neck flexion or just a pillow behind the head can force the tip of the tube downward toward the corina or right mainstem bronchus.  The ideal position is best determined by clinical evaluation and observed improvement in breath sounds.  Continuous monitoring of transcutaneous oxygen and carbon dioxide tension, prior to discharge from the hospital, may also be helpful in defining the best positions for each infant.  Positioning can be  a critical form of therapy for the infant with an airway anomaly that cannot be managed surgically.  This is the case in some vascular abnormalities where the prone or lateral position is necessary (despite other risks) because the heart or great vessels are massively enlarged and impinge on the airway.  The prone or lateral position is also known to improve symptoms is some infants with severe laryngomalacia.

MEDICATION

In the treatment of small airways obstruction beta- (isoetharine, isoproterenol) administered by aerosol can be useful in the absence of overt bronchospasm.  They stimulate goblet cells and mucous glands to produce a thinner, less viscous mucus, and specifically stimulate mucociliary transport.  Some infants with BPD seem to have clinical benefit from adrenergic agents and postural drainage especially for those that have problems of migratory and recurrent atectecsis.  The aerosol treatments are particularly efficacious in lowering bronchomotor tone, increasing airway caliber, and removing respiratory secretions if administration is followed by chest percussion and postural drainage three or four times daily.  Antibiotics may be of benefit in the chronically obstructed airway or instrumented airway if bacterial overgrowth has occurred.   Despite the continued debate about the use of steroid in  chronic airway management and as to the exact mechanism of action of steroids, empirically they have a role in acute and chronic airway management

ACUTE AND CHRONIC

Infants in an NICU not only require management of acute airway problems, but also need consideration of the long-term problems that may be encountered.   Continuing dysfunction may occur because of congenital malformations of the upper, mid, or lower airways; the effects of congenital nonrespiratory disorders, or acquired injuries to the airways.  Design of an appropriate care plan involves anticipation of potential long-term respiratory sequelae of neonatal respiratory tract problems, an appreciation of the fact that the appearance of sequelae may be delayed or modified by postneonatal events. 

SURGICAL MANAGEMENT

Specific interventions depend on the nature, severity, and urgency, of the particular problem.  Conservative management of the airway should be tried initially with oxygen via nasal prongs or mask.  If the obstruction is more significant the airway should be secured with an endotracheal tube.  Rarely will an emergency tracheostomy be necessary to establish an airway in the neonate.  A tracheostomy in the neonate is fraught with dangers not only due to the small size of the patient, small blood volume, but also because of the close proximity of the pleural cupolas of the lungs, and risk of an unrecognized  pneumothrax.  The neonate is more tolerant of prolonged endotracheal intubation, but after a sufficient period of time to see if the basic pathology will or can be corrected,  a tracheostomy should be considered for long term management or for respirator support. 

Significant prolonged obstruction of the nasal cavity requires a tracheostomy for maintenance of the airway long term.  Children with phrenic nerve injury are candidates for long term diaphragmatic pacing, to allow for fairly normal daytime activities.

Tumors of the nasal cavity treatment is protocols are advancing so rapidly it is most appropriate to follow the most successful 

ENCEPHALOCELE 

Intranasal encephaloceles require the combined efforts of the Otolaryngologist and the Neurosurgeon, the first to deal with the nasal component and the latter to close the intracranial and dural defect leading to the nose.  With the advent of advanced endoscopic techniques it would not be surprising to see small forms of these eventually addressed in that manner.  The most common complications of repair are CSF leak, infection, and recurrence43.  And epignathic teratomas are managed in much the same way44.

CHOANAL ATRESIA

Infants with choanal atresia are at severe risk of respiratory failure if the atresia is bilateral, because of the obligate nasal breathing status of infants less than 3 months of age.  In neonates with bilateral atresia, at least one choana must be opened surgically.  Patency of the passage is maintained with a polyvinyl tube (usually a portion of an endotracheal tube cut to appropriate length).  The choanal stent may be removed at three to four months of age, when the infant should be able to breathe by mouth if the surgically opened choana becomes obstructed with mucus.  Definitive repair can be done transpalatally or transnasally, when the child is 2 to 3 years of age, larger and can tolerate blood loss better.  Some argue for earlier complete repair to avoid the risks of tube plugging.  Following the placement of a choanal stent, it is important that the parents receive CPR training and become competent to perform the suctioning required to keep the stent patent and free of secretions.  A portable mechanical suction machine will be necessary for home use.  Infants with unilateral choanal atresia may be managed expectantly, since these children do well unless there is contralateral choanal stenosis or the choana becomes occluded during a respiratory infection.  These infants would also benefit from apnea monitoring.  Unilateral atresia patients frequently have their repair as older children, because of the thick mucus discharge.

PIERRE ROBIN ANOMALY

Those infants who experience only mild respiratory distress may be managed medically with apnea monitors.  Infants with the most severe respiratory obstruction may require tracheostomy to guarantee airway patency for 18 to 24 months; when the growth of the mandible usually provides sufficient airways patency.  Results from surgical labioglossopexy (tongue lip adhesion) have varied, but may allow the infant in borderline cases to avoid a tracheostomy and does not prevent later tracheostomy should the pexy fail.  Hyoid suspension and resection have also been suggested as possible alternative therapies.

VOCAL CORD PARALYSIS

Post-traumatic vocal cord paralysis may be short in duration and require only close medical observation until resolution occurs, especially if the cords rest in a paramedian position.  Aspiration can be a problem and lead to significant apnea and pneumonia.  Unilateral paralysis or paresis is usually tolerated well by the infant and requires no surgical therapy.  However, it warrants regular follow-up with endoscopic evaluation.  This can easily be done using a flexible fiberoptic endoscope  Whenever cord paresis coexists with other medical conditions such as Arnold-Chiari malformation, for which medical or surgical intervention is indicated (e.g., relief of hydrocephalus), such therapy should be implemented promptly.  Surgical relief of the coexisting problem may lead to adequate resolution of the cord paresis.  There is some debate among Neurosurgeons as to whether early posterior fossa decompression might prevent the acquire form of vocal cord paralysis seen in Arnold Chiari Malformation.  Lack of vocal cord sensation in these patients and in those with intracranial events may lead to undetected severe aspiration and life threatening pneumonia.  Persistent bilateral midline cord paresis / paralysis requires a tracheostomy to maintain an airway.

LARYNGEAL WEBS

Thin low grade laryngeal webs may respond to laser treatments, and dilation, but extensive or thick webs require laryngofissure and keel insertion.  Some may even benefit from a laryngotracheoplasty with rib or auricular graft.   All moderate and severe webs require a tracheostomy initially.

SUBGLOTTIC STENOSIS

The early mild cases can respond well to a cricoid split, where the cricoid is cut surgically and a large endotracheal tube stint is placed with the infant kept paralyzed and on a ventilator for seven days.  More severe cases and those involving larger areas require a laryngotracheoplasty, where a rib or auricular cartilage graft is placed with or without a stent.  Periodic endoscopic examinations are necessary to evaluate the repaired airway, to assess the healing process, and when appropriate, to remove granulation tissue.  Laser treatment reduces its mass and allows maintenance of airway caliber following healing of the site.  The ultimate goal, with aggressive management and growth of the airway, is removal of the tracheostomy as early in childhood as possible, with restoration of normal laryngeal and bronchial function. 

Subglottic obstruction may also be due to congenital disorders such as hemangioma, hamartoma, or webs of the laryngeal area.  Surgical removal is ideal, but the extent of the lesion or other complicating medical problems may dictate that the initial approach be conservative, with long-term placement of a tracheostomy tube to assure airway patency.  Once ventilation is established, a definitive medical-surgical plan can be developed.  Subglottic hemangiomas of the capillary type can respond to steroids, but surgical or laser excision of selected cases also has a role. 

TRACHEAL AND BRONCHIAL STENOSIS

Stenotic lesions of trachea and bronchi may be diffuse or segmental.  They may also result from intrinsic reduction in airway caliber or from external compression fro dilated major vessels or aberrant mediastinal structures.  Elucidation of the precise nature of the lesion (e.g., vascular rings or slings) through imaging techniques allows development of a plan for medical and surgical care.  When correction of the underlying cause of airway narrowing is not possible or when it is not sufficient to guarantee patency of the airway, tracheostomy is indicated.  However, lesions in the distal portion of the trachea or limited to the bronchial tree are not always amenable to tracheostomy placement.  In these situations, aggressive medical care directed at pulmonary toilet is indicated to promote growth of the child, manage infection, granulation tissue and maintain adequate ventilation.  In addition tracheomalacia, which is often associated with congenital defects of the tracheal cartilage, leading to lack of support of the trachea and causing partial or total collapse (even during tidal breathing).  The phase in breathing during which tracheal collapse occurs depends on the location of the cartilage anomaly.  Inspiratory stridor occurs when the defects are confined to the extrathoracic trachea, whereas expiratory stridor occurs when the defects are confined to the intrathoracic trachea.  When the tracheal narrowing is severe and / or the tracheal cartilage defect comprises a large portion of the trachea, severe tracheal obstruction occurs and seriously compromises ventilation45.  Treatment of life-threatening obstruction includes establishment of a patent airway with placement of an artificial airway (tracheostomy tube) to bypass the tracheal obstruction.  The entire anterior wall of the tracheal can be reconstructed with rib or pericardium or Gortex.  New wire and silastic stent that coil open and stretch the narrowed trachea open are now available.

TRACHEOESOPHAGEAL FISTULA

Surgical correction of esophageal atresia and tracheoesophageal fistula achieves anatomic but not "functional" restoration of the involved passages.  Infants with these conditions bear a number of functional disabilities after surgery, which vary in the extent of their clinical expression.  Residual upper airway obstruction is experienced by some infants because their tracheas are narrower than normal, and have an altered mucus flow pattern.  The esophageal motility is discontinuous at the anastamosis site, because of the disruption of the autonomic myenteric plexus.         

CONCLUSION

The neonatal airway can be complex and treacherous, and thus demands the utmost of attention by the Neonatologist and the Otolaryngologist working together with Respiratory care and a dedicated nursing staff. Each day a new cause of obstruction is documented and nature will always bring new challenges, that must be met with a perspective of what has been known, but also with an acceptance of and search for new management ideas. 

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33.  Terris MH, Pransky SM, Airway compromise secondary to vascular compression in a   neonate, Int J Pediatr Otorhinolaryngol, Jan 1994, 28(2-3) p193-7.

34.  Heck HA, Moore HV, Double aortic arch and tracheomalacia, Tex Heart Inst J 1993,   20(2) p126-9.

35.  Cohen SR, Geller KA, Birns JW, Thompson JW, Foregut cysts in children. Diagnosis and  management. Ann Otol Rhinol Laryngol 1982; 91:622-27.

36.  Hiyama E, Yokoyama T, Surgical management of Tracheal agenesis, J Thorac    Cardiovasc Surg, Nov 1994, 108(5),p830-3.

37.  Filler RM, Messineo A, Severe tracheomalacia associated with esophageal atresia, J   Pediatr Surg, Aug 1992, 27(8)p1136-40.

38.  Smith SP, Berkowitz E, Acquired Subglottic cysts in infants, Arch of Otolaryngol Head   and Neck Surg, Apr 1994 120(4) 454-8.

39.  Stamos JK, Rowley AH, Timely diagnosis of congenital infections, Pediatr Clin of North   Am, Oct 1994, 41(5) p1017-33.

40.  Bohman L, Mancuso A, Thompson JW, Hanafee W, CT of nasopharynx normal and  variants of normal.  Radiol 1980;137:113-21.

41.  Bohman L, Mancuso A, Thompson JW, Hanafee W,  A CT approach to benign  nasopharyngeal masses. Amer Jrnl Roentgen 1981;136:137-80.

42.  Tolley NS, Ford G, Commins D, The management of neonatal rhinitis, Int J Pediatr   Otorhinolaryng Nov 1992, 24(3) p253.

43.  Date I, Yagyu Y, Long term outcome in surgically treated encephalocele, Surg Neurol,   Aug 1993, 40(2) p125-30.

44.  Langer J.C. Tabb T, Thompson P. Management of prenatally diagnosed tracheal    obstruction: access to the airway in utero prior to delivery, Fetal Diagnos Ther, 1992,   7(1) p12-6.

45.  Reiterer F. Eber E. Management of severe congenital tracheobronchialmalacia Pediatr   Pulmonol Jun 1994, 17(6) p401-3.