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Nasal

Obstruction

in the Pediatric

Patient

Charles

M. Myer

Ill, MD, and

Robin

T. Cotton,

MD, FACS,

FRCS(C)

From the Department of Otolaryngology and Maxillofacial Surgery, University of Cincinnati

College of Medicine, Cincinnati

ABSTRACT. Early signals of pathologic causes of nasal obstruction in childhood may pass unnoticed by the un-suspecting physician because these signals mimic

innoc-uous problems such as the common cold, sinusitis, and

allergic rhinitis. The hope for early recognition of the more serious causes of nasal obstruction in children de-pends upon a high degree of suspicion. Some of the

common and uncommon causes of nasal obstruction are enumerated by categorizing the possible etiologies into congenital, traumatic, iatrogenic, inflammatory, and neo-plastic classifications. With a systematic approach that utilizes history, physical examination, and special

diag-nostic studies, misdiagnosis can be avoided and treatment initiated more rapidly and effectively. Pediatrics 1983; 72:766-777; nasal obstruction, rhinitts.

The human nose has multiple physiologic func-tions. Besides serving as a vocal resonator and as the site of olfaction, the nose serves several pur-poses for the respiratory system, including the warming, filtration, and humidification of inspired air. Diseases of the nose interfere with these func-tions and may produce symptoms referable to them. In addition to nasal obstruction, patients may com-plain of epistaxis, anosmia, hyponasality, or cos-metic deformity. Combining a thorough history and physical examination with appropriate radio-graphic and bacteriologic studies, a meaningful dif-ferential diagnosis may be developed in the evalu-ation of nasal obstruction in the pediatric patient. By categorizing the possible etiologies of nasal ob-struction into congenital, traumatic, iatrogenic, in-flammatory, and neoplastic classifications, one can readily diagnose and successfully treat many nasal disorders.

Received for publication Nov 30, 1982; accepted March 30, 1983.

Reprint requests to (C.M.M.) Department of Otolaryngology and Maxillofacial Surgery, University of Cincinnati College of Medicine, Cincinnati, OH 45267.

PEDIATRICS (ISSN 0031 4005). Copyright © 1983 by the

American Academy of Pediatrics.

CONGENITAL NASAL OBSTRUCTION

Choanal Atresia

Posterior choanal atresia is, simply, obliteration of the posterior nasal aperture. It is seen in approx-imately one in 8,000 births and a familial tendency has been noted. A definite etiology of choanal atre-sia is not known. During the 4th week of embryonic life, the primative nasobuccal membrane fails to rupture; this results in the persistence of an atretic plate and, consequently, posterior choanal atresia. The stenosis is bony rather than membranous in about 90% of all cases. It is more commonly seen in females and is most often unilateral.’ Associated congenital anomalies have been reported and the incidence ranges as high as 50% in the cases with choanal atresia. Among anomalies reported are Treacher Collins syndrome; facial, nasal, and pal-atal deformities; polydactylism; congenital heart disease; coloboma of the iris and retina; mental retardation; and malformations of the external ear. Less frequently occurring conditions are esophageal atresia, craniosynostosis, tracheoesophageal fistula, and meningocele.2

The clinical picture is classic in infants with bilateral atresia. Complete obstruction of the nasal airway is marked by strenuous but unsuccessful efforts at breathing in these obligate nasal breath-ers. Cyanosis develops until the infant is made to cry and the obstruction is bypassed. Once the crying stops, however, the mouth closes and a pattern of

I’cyclical obstruction b&me established. The

di-(

agnosis of choanal atresia is suspected when a No. . 5 or No. 6 French feeding catheter cannot be passed

.

through the nose into the nasopharynx a distance . . of at least 32 mm. Confirmation may be obtained

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surgical techniques have been described. Transan-tral, transnasal, and transpalatal approaches all have their proponents depending on the patient’s

age and the type of stenosis present. Silastic nasal stents are routinely left in place after any procedure for a variable period of time. Restenosis postoper-atively is not common.3

Posterior Choanal Stenosis

Fig 1. Bilateral atresia plate prevents dye from entering

nasopharynx.

Fig 2. Chronic right-sided rhinorrhea prompted discov-ery of unilateral choanal atresia in 9-year-old girl. Atresia plate is labeled A.

later life when symptoms of unilateral nasal ob-struction and rhinorrhea are investigated.’

Immediate therapy in the neonatal period in-volves the placement of an oral airway or McGovern nipple and the institution of gavage feedings. The timing of definitive surgical repair is controversial. Because the ability of the infant to mouth breathe may take several months to develop, surgical cor-rection is usually instituted prior to discharge from

the hospital. Few parents or physicians would be comfortable discharging a newborn with an oral airway as the sole means of ventilation. Multiple

Congenital posterior choanal stenosis presents as a narrowing of the posterior choana representing an incomplete choanal atresia or a hypoplastic na-sopharynx. The hypoplastic nasopharynx is usually associated with a more generalized skull deformity such as seen in craniofacial dysostosis or mandi-bulofacial dysostosis. Congenital stenosis of the posterior choana occurs with airway obstruction from birth. If severe, it may mimic choanal atresia. With less severe stenosis, the infant may experience symptoms of airway obstruction only during

feed-ing. Excessive mucoid discharge may be the only symptom in mild forms of posterior choanal ste-nosis. Lateral radiographs with contrast material placed alternately in each nasal chamber are some-times useful to define the area of stenosis. CT may also be ofbenefit. Because the nasal cavity normally enlarges within weeks or months, the condition is

probably best treated symptomatically.’

Tornwaldt’s

Cyst

The pharyngeal bursa is a diverticulum-like structure seen in 3% of the general population; it lies in the midline of the posterior wall of the nasopharynx just superior to the adenoid pad. Its origin is not clearly understood, but may be related to the formation of a potential space between the pharyngeal epithelium and notochord remnants. The lesion is congenital but the peak incidence of clinical symptoms of Tornwaldt’s cyst is generally around the second or third decade of life. Inflam-mation of the opening of this bursa results in cyst formation and subsequent infection of the cyst con-tents. Symptoms occur only when the space be-comes infected. The principal symptoms are per-sistent occipital headaches accompanied by an an-noying postnasal discharge. Nasopharyngeal ex-amination shows a crusted midline mass which may appear cystic. Lateral soft tissue radiographs reveal a sharply circumscribed soft tissue mass high in the posterior nasopharynx. Therapy consists of either local excision down to the periosteum or wide mar-supialization.4

Malformations

of the Nose

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first branchial arch. The major contribution to the dorsum of the nose is from the frontal prominence. At about the 9th week of fetal life, the septal process growing inferiorly meets the two palatine processes growing medially. Fusion of these three processes in the midline progresses posteriorly from the in-cisive foramen to form the primary palate. The nasal cavity is thus separated from the oral cavity

whereas the nasal passages are divided into halves. Any problem with the proper timing sequence em-bryologically can lead to a malformation.” These malformations range from complete nasal absence to partial absence, clefts, and facial dysostosis. Three deformities of the nose are typically seen in association with a cleft lip. They are sometimes present in the absence of a cleft lip. The triad

characterizing the cleft lip-nose deformity includes nasal tip deformity, dorsal displacement of the dome, and buckling of the alar cartilage.’

Dermoid

Dermoid cysts and sinuses of the nose are rela-tively rare. One report indicates that they represent about 13% of head and neck dermoids.6 Their pres-entation is usually at birth or within the first few months of life. Two major theories have been pos-tulated to explain the development of these lesions. The cranial origin theory of dermoid cysts and sinuses is based on the faulty recession of dura mater from the prenasal space during normal em-bryogenesis. In contrast, the superficial inclusion theory is based on the concept that ectoderm is trapped submucosally to form a cyst when the lateral nasal processes fuse. These lesions most frequently occur as progressively enlarging masses in the midline of the nose. One should suspect the possibility of a dermoid cyst whenever there is a discrete swelling of the nose in a newborn or infant. The cysts are generally located in the nasal midline and frequently cause distortion of the normal nasal architecture. A sinus tract is often present. If se-baceous material can be expressed from the cuta-neous pit, or if hairs are present, one should be suspicious of the diagnosis of dermoid cyst. One should also be cognizant of possible extension of the dermoid into the cribriform plate region as well as intracranially. Therapy involves complete sur-gical extirpation as described by Sessions7 (Fig 3).

Encephalocele

Nasal encephaloceles are extrusions of menin-geal-lined brain substance that communicate freely with the intracranial ventricular system and sub-arachnoid space. The lesion appears to be the result of defective closure of the anterior neuropore that

Fig 3. Surgically resected congenital midline nasal mass (A) confirmed by histopathology to be a dermoid cyst.

occurs at the beginning of the 4th week of embry-onic life. The general incidence is approximately one in 4,000 births. Of these encephaloceles, 60% are seen externally over the bridge of the nose whereas 30% are intranasal. Ten percent of nasal

encephaloceles have both intranasal and external components. It should be remembered that nasal

obstruction almost certainly occurs when these masses appear at the skull base. In the newborn, this may be an emergent situation that requires an immediate tracheostomy. The lesions most com-monly present as nasofrontal or nasoethmoid swell-ings which exhibit a slow growth pattern. Menin-gitis is certainly a possibility if inadvertent intrana-sal surgical manipulation of an encephalocele is performed and copious rhinorrhea results. Biopsy of these lesions is never indicated. Surgical excision through an intracranial or combined intracranial and extracranial approach is the only acceptable mode of therapy.’

Glioma

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identical with that of the encephalocele and is secondary to faulty closure of the anterior neuro-pore. In approximately 20% of the cases, an intra-cranial connection persists through a fibrous stalk. The majority of these lesions occur intranasally and cause nasal obstruction. They arise from the lateral nasal wall and are often misdiagnosed as a nasal polyp. As such, they may be inadvertently biopsied. If an intracranial connection exists, CSF leakage may occur with the risk of meningitis. Definitive therapy is directed at complete surgical removal. Controversy exists as to whether an intra-cranial procedure is always necessary.8

Teratoma

Teratomas are congenital masses with

deriva-tives of all three germ layers. This is to be differ-entiated from dermoids that contain ectoderm and mesoderm only. They have been found to contain cartilage, bone, muscle, thyroid, and glial tissue. Lesions appear to arise from embryonic rests of tissue that fail to organize properly or may even represent an incompletely developed twin of the host. They exhibit rapid growth and, in this regard, behave as a true neoplasm. They are most com-monly recognized early in infancy. Radiographic evaluation should always be obtained before at-tempting surgical removal to exclude an intracra-nial component of the lesion. Unlike teratomas in other locations, those arising in the nasopharynx do not appear to have as great a potential for malignant degeneration. Malignant degeneration has been known to occur, however, especially in older children and young adults. In this group, teratocarcinomas arise high in the nasal cavity and are associated with a poor prognosis secondary to rapid intracranial extension.9

TRAUMATIC

NASAL

OBSTRUCTIONS

Blunt or Penetrating

Trauma

Nasal obstruction following blunt or penetrating

trauma to the midface is not uncommon. Disloca-tion of the nasal bones and septum results in an anatomic obstruction of the nasal passages. Surgi-cal correction utilizing a septoplasty or closed re-duction is indicated for symptomatic airway oh-struction. A formal rhinoplasty should be post-poned until adolescence. It should be remembered that unrecognized and untreated septal hematomas may result in dissolution of the nasal septal carti-lage in as little as 48 hours. Clotted blood collects between the mucoperichondrium and septal carti-lage; this results in deprivation of the blood supply of the septal cartilage with subsequent enzymatic

breakdown of the septum. Prevention of sequela, such as a saddle nose deformity, involves rapid recognition of the problem with immediate surgical drainage and appropriate antimicrobial therapy.’#{176}

Nasal septal deviation occurs in approximately 1% of all neonates. It is most commonly seen fol-lowing vaginal delivery and is felt to be secondary to either faulty application of forceps or traumatic passage through the birth canal. It has also been

described following cesarean section but the factors responsible for this are unknown. One becomes suspicious of this deformity when the newborn ex-hibits a tilted columella, deviation of the nasal tip, or asymmetry of the nasal alae. Intranasal manip-ulation with a small instrument can be used to confirm the diagnosis when in question. Sponta-neous correction of a septal deformity appears to take place when the septum has not been displaced from the vomer grove. Ifdisplacement has occurred, a closed reduction should be performed within the first week of life.1

Foreign

Body

Intranasal foreign bodies may also occur with airway obstruction. A thorough examination often reveals the presence of a foreign body in the nose of a child who has unilateral purulent rhinorrhea and complains of nasal blockage. Purulent dis-charge may obscure the foreign body and the nose should be thoroughly suctioned prior to inspection. Topical vasoconstrictive agents will also facilitate intranasal examination prior to attempted removal of the foreign body. General anesthesia may be necessary in those children who are unable to co-operate sufficiently. In any child with a nasal for-eign body, the opposite nostril and both external auditory canals should be inspected for a concomi-tant foreign body.

IATROGENIC

NASAL

OBSTRUCTION

Nasopharyngeal

Stenosis

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Fig 4. Region of nasopharyngeal stenosis (A) secondary to distortion and scarring of soft palate (B) and posterior pharyngeal wall (C) following tonsillectomy and adenoidectomy.

lateral adenoid bands, revision surgery, and the tendency to form keloids or cicatrix formation.’1 Other conditions reported to have caused nasopha-ryngeal stenosis include: caustic burns, diphtheria, and systemic lupus erythematosus. Multiple types of surgical repairs have been described for this abnormality.’2

Surgical

Correction

of Velopharyngeal

Insufficiency

Velopharyngeal insufficiency is the inability of the velopharyngeal sphincter to function effectively during connected speech; this results in hyperna-sality and nasal speech. Speech therapy, obturators, and various surgical procedures have all been uti-lized as methods to diminish velopharyngeal escape. Two of the more common surgical procedures uti-lized for correction of velopharyngeal insufficiency in this country are posterior pharyngeal wall aug-mentation and palatopharyngoplasty with a supe-riorly based pharyngeal flap. In either of these operations, nasal airway obstruction may result. Particular attention must be paid to the mainte-nance of adequate lateral pharyngeal ports for the maintenance of nasal respiration.’3

Rhinitis

Medicamentosa

Rhinitis medicamentosa may be seen as a result of the prolonged administration of topical nasal decongestants. Regular use of these substances for longer than 1 week will result in a phenomenon

known as rebound nasal mucosal dilation. A cyclical pattern is established whereby the patient becomes increasingly dependent on nose drops because the relief he experiences from their usage diminishes with continued use. Although the actual incidence

of rhinitis medicamentosa is unknown, it is felt to be common in patients with chronic nasal obstruc-tion in such disorders as nasal septal deviation and nasal polypoisis.

The patient commonly has a thick, reddened, edematous nasal mucosa and complaints of inter-mittent nasal obstruction. The diagnosis, which has been suspected on the basis of the patient’s history, is confirmed when topical 4% cocaine is ineffective in the production of vasoconstriction of the nasal mucosa. Therapeutic intervention must be accom-panied by patient education. The patient must ac-cept the responsibility for his present condition and understand his role in its alleviation. Topical nasal vasoconstrictors must be eliminated initially; when used in the future, their use must be limited to less than seven days. During this withdrawal period symptomatic relief may be provided for the patient by several methods. Partial relief is gained from the administration of an antihistamine-decongestant

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follow-up to prevent a reexacerbation of their con-dition.

A common side effect of certain systemically administered medications is nasal stuffiness. Tur-binate enlargement in this situation appears to be caused by a primary effect of the medication on the neural and vascular supply to the turbinates. This is a less frequent cause of rhinitis medicamentosa than topical medications but it is treated in a sim-ilar way. Those agents most commonly implicated include: antihypertensives (reserpine, hydralazine, guanethidine, methyldopa, prazosin), 3-blockers (propranolol, nadolol), and antidepressants (thior-idazine, chlordiazepoxide, amitriptyline, perphena-zine).’4

INFLAMMATORY

NASAL

OBSTRUCTION

Infectious Rhinitis

Nasal obstruction is most often found as a symp-tom of infectious rhinitis. Inflammation of the na-sal mucosa is commonly part of a generalized upper respiratory tract infection which may include na-sopharyngitis and sinusitis (Fig 5). The condition may be suppurative or nonsuppurative and may be classified as acute, subacute, or chronic. Immuno-deficiency may be a predisposing factor. Therapy must be tailored to the specific conditions present and it should be remembered that the most common bacterial organisms responsible for acute sinusitis are the pneumococcus and Haemophilus influenzae. Anaerobes play an important role in the production of chronic sinusitis. Nasopharyngeal cultures have

Fig 5. Endoscopic view of posterior choana demonstrat-ing edematous turbinates (A) and purulent rhinorrhea (B) as seen with infectious rhinitis. Soft palate (C) is labeled for orientation.

little significance in the identification of those or-ganisms responsible for sinusitus. Aggressive suc-tioning is important in the treatment of newborns

because of obligate nasal breathing.”‘

Retropharyngeal Abscess

An unusual cause of nasal obstruction, retro-pharyngeal abscess, is primarily a disease of young childhood. Lymph nodes in the retropharyngeal space become infected most commonly in acute infections of the nose, sinuses, or nasopharynx. Progression of the infection leads to suppuration and subsequent abscess formation. Although retro-pharyngeal abscess infrequently presents with na-sal obstruction, it may do so when nodes high in the nasopharynx are involved. More commonly, however, the patient presents with a pharyngitis and cervical adenopathy. Other complaints com-monly seen include meningismus, intermittent stri-dor, dysphasia, and irritability. Lateral soft tissue radiographs commonly show widening of the soft tissues between the pharyngeal air column and the bodies of the cervical vertebrae. Normal variants must not be confused with pathologic conditions. Inspiratory and expiratory films should be used to delineate the normal soft tissue bulge seen in ex-piration. Treatment of these patients involves in-cision and drainage and should be carried out under general anesthesia with an endotracheal tube in place. Appropriate antibiotic therapy is also mdi-cated. Mediastinal extension of the suppurative process should always be excluded by careful ex-amination of the chest roentgenogram as well as maintaining a high degree of clinical suspicion.’6

Allergic

Rhinitis

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anti-mucopurulent discharge are the hallmarks of this syndrome, which is most commonly seen in the late fall and winter months. Nasal cytology preparations are usually devoid of eosinophils but show sheets of neutrophils. The condition usually resolves spon-taneously before children reach the age of 10 years. Symptomatic relief may be obtained with the use of a mild decongestant.’7

Atrophic Rhinitis

Fig 6. Mucoperiosteal thickening in maxillary sinuses, a typical radiographic finding in allergic rhinosinusitis. Small air-filled region of sinus (A) is indicated.

histamine-decongestant therapy, desensitization injections, systemic corticosteroids, and, more re-cently, the use of intranasal steroids.’7

Vasomotor

Rhinitis

Vasomotor rhinitis is best thought of as a hyper-active cholinergic response that results in turbinate engorgement and hypersecretion. It is a diagnosis of exclusion because its symptoms mimic most other nasal disorders that cause obstruction. Vas-omotor instability is marked by alternating nostril congestion and is triggered by several factors. These include recumbency, alcohol consumption, temper-ature and humidity changes, and nonspecific envi-ronmental irritants. Rhinorrhea is not common, but postnasal discharge is a frequent complaint. Sinusitis and otitis media may be seen concurrently in these patients.

Therapeutic intervention for this problem is gen-erally not satisfactory. Avoidance of precipitating factors is usually of some benefit. Likewise, the judicious use of systemic and topical decongestants

is often beneficial. Antihistamines, as well as topi-cal and systemic corticosteroids, however, may ac-tually aggravate existing symptoms.”‘

Chronic

Rhinitis

of Childhood

Chronic rhinitis of childhood is a self-limited vasocongestive syndrome seen in children less than 6 years of age. Perennial nasal congestion and

Atrophic rhinitis is an unfortunate condition in which severe nasal obstruction is seen with physi-ologically patent nasal passages and a foul odor emanating from the nose. Multiple etiologies have been proposed, including the normal aging process, excessive removal of nasal mucosa, and a previously existing Wegener’s granulomatosis. The nasal smear is unremarkable unless there is secondary infection present. The turbinates are quite small and consist of a thin mucosa with few mucus-producing cells. Therapy is basically symptomatic and consists of topical lubrication and antibiotics for infectious processes. Nostril closure has been advocated by certain authors in the treatment of this condition.’7 This condition is exceedingly rare in children.

Nasal Polyps

A history of progressive nasal obstruction in chil-dren with allergic rhinitis, asthma, or chronic pu-rulent nasal discharge may suggest nasal polyps. On physical examination, nasal polyps may be seen above the inferior turbinate as gray, glistening masses arising from the ethmoid labyrinth. They may appear translucent and are often associated with a mucoid discharge. Palpation of the polyps with a small probe may aid in differentiating these growths from the normal turbinate.”‘ In addition, the ability to pass a probe medial to these masses distinguishes them from basal encephaloceles. Their etiology is uncertain, but appears to be as-sociated with chronic inflammatory processes of both infectious and allergic etiologies.8

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of this frequency, a sweat chloride test should be seriously considered whenever one evaluates a child with nasal polyps.’8

Therapeutic considerations in nasal polyposis are the same regardless of whether the child has cystic fibrosis or nasal polyps secondary to chronic in-flammation. Symptomatic relief is obtained by re-peated intranasal polypectomies. Topical steroid sprays have recently been utilized to prolong the symptom-free interval. An ethmoidectomy is rarely indicated in the pediatric patient.”‘

An antral-choanal polyp is a specific type of nasal polyp occasionally seen in children. It originates in the maxillary sinus and, as the polyp enlarges, it protrudes from the sinus ostium into the middle meatus of the nose. It may eventually fill the entire middle meatus with extension beyond the posterior end of the inferior turbinate to occlude the ipsilat-eral posterior choana. With continued growth, the mass may present below the palate in the orophar-ynx. Voice changes may be secondary to mechanical interference with palatal function, or the patient may complain of the sensation of a mass in the throat and gagging. Paranasal sinus radiographs generally reveal opacification of an expanded max-illary antrum associated with a nasopharyngeal mass (Fig 7, top). Confirmation may be made at nasopharyngoscopy. Therapy consists of complete surgical removal through a sublabial antrostomy in combination with an intranasal excision (Fig 7, bottom).’9

A recently described condition in children is known as Woake’s syndrome. This phenomenon

consists of severe recurrent nasal polyposis during childhood with broadening of the nasal dorsum, the production of tenascious nasal secretions, frontal sinus aplasia, and bronchiectasis. The syndrome appears to be hereditary. It is speculated that an inborn defect causing excessively viscous nasal Se-cretions is responsible for the production of the remaining symptoms of the syndrome. The condi-tion should be distinguished from the other known etiologies of nasal polyposis in children including cystic fibrosis, Kartagener’s syndrome, recurrent sinusitis, and aspirin intolerance. Because only four patients with this syndrome have been described, the long-term prognosis is not known. Therapy is directed toward symptomatic relief as previously described.20

Adenoid

Hypertrophy

Obstruction of the posterior nasal choana by adenoid hypertrophy, is a common cause of nasal stuffiness. Mouth breathing, noisy respirations while awake, and loud snoring are all symptoms commonly found in these individuals. An adenoid

facies is characteristic and consists of an open mouth, flattened nose, small or underdeveloped nostrils, short upper lip, thick everted lower lip, and a vacant or disinterested expression.2’

A distinct syndrome of upper airway obstruction with secondary cardiovascular effects has been de-scribed in recent years. These patients with periph-eral sleep apnea have extremely noisy breathing and excessive daytime sleepiness. The signs of oh-struction can be made worse, or even emergent, by administration of sedatives, supine positioning, or acute upper airway infections. A thorough medical investigation often shows hypertrophy of the right ventricle, congestive heart failure, and hypercapnia. The etiology of these changes is marked hypertro-phy of the tonsils and adenoids sufficient enough to cause respiratory tract obstruction and hypoxia. Therapy involves bypass of the obstruction, gener-ally by removal of the tonsils and adenoids. In acute situations, a nasopharyngeal airway may be uti-lized. Tracheostomy may be required when severe hypopharyngeal collapse is present in addition to adenotonsillar hypertrophy.22

NEOPLASMS

True neoplasms of the nasal cavity are rare and comprise less than 0.3% of the tumors of the body. Included herewith are some of the more significant neoplasms that produce nasal obstruction in the pediatric age group.23

Benign

Tumors

Hemangiomas. The most common benign tumors

found in neonates are hemangiomas and hemangi-olymphangiomas. They may be divided into two subgroups, papular hemangiomas and cavernal he-mangiomas. The former appears as a papular growth on the nasal skin or vestible and exhibits rapid growth with occasional hemorrhage. Most undergo spontaneous resolution over a period of several years. Cryosurgery has been used to de-crease the size of these lesions but a formal surgical procedure is rarely indicated.

Cavernal hemangiomas are often located in the nasal tip of neonates. They tend to grow rapidly and show little tendency toward involution. Be-cause of this, surgical intervention at approximately 6 months of age is indicated. Radiation therapy has little role in the treatment of these neoplasms.24

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prolifera-T

4A

tion of a local group of blood vessels in association

with an increase in hydrostatic pressure. These lesions present as polypoid or sessile masses and can usually be diagnosed on their gross clinical appearance.2529’3’2 Most patients have epistaxis and nasal obstruction, generally of less than 6 months duration.

In spite of its apparent traumatic etiology, nasal

mucosal hemangiomas tend to behave clinically as true neoplasms. Although a majority of congenital hemangiomas regress spontaneously, other types of hemangiomas, including those of the nasal septum, require some form of definitive therapy. The best method of treatment appears to be wide local exci-sion of the mass together with a cuff of underlying mucosa and perichondrium. The defect is allowed

&T.1

T,:,

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to granulate. Therapy must obviously be individu-alized and locally infiltrative tumors require more radical surgery.26

Juvenile Nasopharyngeal Angiofibroma. The ju-venile nasopharyngeal angiofibroma often appears secondarily in the nasal cavity as a result of its

growth from the nasopharynx. This histologically benign growth in adolescent males arises from the fibrocart.ilaginous tissue overlying the upper cervi-cal vertebrae. Its growth appears to be accelerated

at. puberty. The neoplasm causes recurrent epi-staxis, rhinorrhea, and nasal obstruction. It appears

clinically as a reddish-brown, smooth mass protrud-ing from the nasopharynx (Fig 8). There is debate concerning treatment. Biller et al27 found that small tumors can be surgically extirpated after arteriog-raphy and embolization. Fitzpatrick et a128, how-ever, advocate radiation therapy as the treatment of choice, especially for tumors with intracranial extension.

Miscellaneous Tumors. Other benign neoplasms of childhood may present in the nose and the na-sopharynx. These include craniopharyngiomas,

chordomas, lipomas, chondromas, hemangioperi-cytomas, neurolemmomas, neurofibromas,

rhab-domyomas, and pleomorphic adenomas of minor salivary gland origin.9

Malignant

Tumors

Nasopharyngeal neoplasms as a whole are diffi-cult to diagnose at an early stage. Local symptoms

occur first but they are often overlooked because of

their common occurrence in normal children. As the tumors expand in the nasopharynx, they may block the eustachian tube and give rise to a middle ear effusion. Obstruction at the posterior choana causes nasal discharge which may be mucopurulent. or bloody. The voice quality is often described as hyponasal due to the lack of normal nasal reso-nance. Enlarged cervical lymph nodes or cranial nerve abnormalities may also be present. The

fol-lowing discussion describes those malignancies most commonly responsible for nasal obstruction

in children.9

Lymphoma. Hodgkin’s and non-Hodgkin’s lym-phoma are the most common malignancies of the

nasopharynx in children. The general clinical pic-ture usually allows the diagnosis to be made al-though some patients may have nasal obstruction when the nasopharynx is initially involved.

Radia-tion therapy and chemotherapy are employed in treatment.9

Rhabdomyosarcoma. Rhabdomyosarcomas

com-prise the single largest group of malignant, sup-porting tissue neoplasms of the head and neck in children. About 70% of all rhabdomyosarcomas of

the head and neck occur in patients less than 12 years of age. The tumors essentially recapitulate

the embryogenesis of skeletal muscle and have 5ev-eral histologic forms. Embryonal rhabdomyosar-coma is the most common form in children.

Symptoms are dependent upon the site of tumor

origin and its growth pattern. Tumors may arise in

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either the nasal cavity or the nasopharynx in ad-dition to other head and neck locations (Fig 9). The nasopharyngeal tumors may cause local symptoms such as pain, hearing loss, nasal obstruction, chronic nasal discharge, or hyponasality. Cervical adenopathy or cranial nerve symptoms are a poor prognostic sign. Extension of disease into the mid-dle ear and mastoid may produce facial paralysis.

Survival rates for rhabdomyosarcoma are poor. In spite of aggressive surgical therapy in combina-tion with adjuvant chemotherapy and radiation

therapy, a 10% 5-year survival rate can generally be expected with tumor involving the nasophar-ynx.2522m)

Nasopharyngeal Carcinoma. In the pediatric age group, carcinoma of the nasopharynx is rare. Squa-mous cell carcinoma is the most common type and

its histologic picture is characterized by normal appearing lymphocytes in combination with large epithelioid cells. This relationship has caused some authors to classify these lesions as lymphoepithe-liomas. The etiology is unknown, but both genetic and environmental factors are believed to play a role in its development. In addition, patients with nasopharyngeal carcinoma have shown elevated ti-ters of anti-Epstein-Barr virus antibodies which decrease with successful therapy. The significance of this is unknown.

As mentioned previously, the presenting symp-toms of nasopharyngeal neoplasms are multiple and nonspecific. Only by formal endoscopy under gen-era! anesthesia can the tumor be adequately as-sessed and biopsied. Cervical metastases occurs in 70% of all patients; 39% have bilateral metastases. Skull base erosion also occurs in a high percentage

Fig 9. Rhabdomyosarcoma of temporal bone (A) which occurred with nasal obstruction due to nasopharyngeal extension (B).

of patients, especially those with cranial nerve

pa-ralyses. Radiation therapy is the treatment of choice and consists of high-dose radiation to both the primary tumor and both sides of the neck.

Radical neck dissection should be considered when

there is control of the primary tumor but there

remains residual disease in the neck. Chemotherapy and cryotherapy have occasionally been used for failures of conventional therapy. Although the over-all 5-year survival rate is 35%, it is felt that younger patients have a somewhat increased survival over that of the general population.9

Esthesioneuroblastoma. The

esthesioneuroblas-toma is an unusual malignancy which arises from the nasal olfractory epithelium. This specialized region is confined to the upper surface of the su-perior turbinate, the uppermost part of the nasal

septum, and the under surface of the cribriform

plate. As a result, esthesioneuroblastomas take their origin from the upper third of the nasal sep-tum and the lateral nasal wall. The tumor is seen in most age groups but does appear to have its peak incidence in the second decade. Symptoms, again, are nonspecific and similar to those seen with other nasal and nasopharyngeal neoplasms. Diagnosis may be difficult because a small biopsy specimen may be confused with sarcomas or carcinomas.

Therapy for these tumors has been disappointing. Neither radical surgery nor radiation, whether given singly or in combination, has been completely effective in tumor control. Inadequate local excision invariably leads to local recurrence. Although 5-year survival rates range from 45% to 67%, there does seem to be local recurrence in about half of the cases and distant metastases appear in about

25% of cases.25’4’346

SUMMARY

An attempt has been made to classify the various causes of nasal obstruction in the pediatric patient. The schema presented demands that the physician maintain an index of suspicion whenever con-fronted with this problem. He must not reflexly accept the complaint of nasal obstruction as a symptom of an upper respiratory tract infection. By approaching the problem in an orderly fashion,

the physician can greatly improve his success rate in the rapid diagnosis and treatment of nasal ob-struction in children.

REFERENCES

1. Jaffe BF: Classification and management of anomalies of the nose. Otolaryngol Clin North Am 1981;14:989-1004

2. Hall BD: Choanal atresia and associated multiple anomalies.

J Pediatr 1979;95:395-398

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airway obstruction in craniofacial anomalies. Otolaryngol

C/in North Am 1981;14:1005-1017

4. Toomly JM: Cysts and tumors of the pharynx, in Paparella MM, Shumrick DA (eds): Otokiryngology. Philadelphia, WB Saunders, 1980, vol 3, pp 2323-2324

5, Davies .1: Embryology and anatomy of the head, neck, face, palate, nose and paranasal sinuses, in Paparella MM, Shum-rick DA (eds): Otolaryngology. Philadelphia, WB Saunders, 1980, pp 103-116

6. New GB, Erich JB: Dermoid cysts of the head and neck.

Surg Gynecol Obstet 1937;65:48-55

7. Sessions RB: Nasal dermal sinuses-new concepts and ex-planations. Laryngoscope 1982;92(suppl 29):1-28

8. Hughes GB, Sharpino G, Hunt W, et al: Management of the congenital midline nasal mass: A review. Head Neck Surg 1980;2:222-223

9. Snow JB Jr: Neoplasms of the nasopharynx in children.

Oto/aryngo/ C/in North Am 197;10:11-24

10. Myers EN: Finding the cause of nasal obstruction. J Respir I) 1981;2(12):107-118

11. Lehmann WB, Pope TH Jr, Hudson WR: Nasopharyngeal stenosis. Laryngoscope 1968;78:371-385

12. McDonald TJ, Devine KD, Hughes AB: Nasopharyngeal stenosis following tonsillectomy and adenoidectomy. Arch

Otolaryngol 1973;98:38-41

13. Cotton R, Nuwayhid NS: The surgery of speech, in (Papa-rella MM, Shumrick DA (eds): Otolaryngology. Philadelphia, WB Saunders, 1980, pp 2170-2191

14. Mabry RL: Rhinitis medicamentosa: The forgotten factor in nasal obstruction. South Med J 1982;75:817-819

15. Zeiger RS, Schatz MD: Chronic rhinitis: A practical ap-proach to diagnosis and treatment: I: Diagnosis. Immunol

Allergy Pract 1982;4:17-32

16. Seid AB, Dunbar JS, Cotton RT: Retropharyngeal abscesses in children revisited. Laryngoscope 1979;89:1717-1724

17. Jacobs RL: A practical classification of chronic rhinits. J Respir Dis 1981;2:20-35

18. Kramer RI: Otorhinolaryngologic Complications of Cystic Fibrosis. Otolaryngol Clin North Am 1977;10:205-208 19. Crowe JE, Sumner TE, Ranquist NA, et al: Antrochoanal

polyps. South Med J 1982;75:674-676

20. Kellerhals B, de Uthemann B: Woakes syndrome: The prob-lems of infantile nasal polyps.

mt

Pediatr Otorhinolaryngol

1979;1:79-85

21. Kornblut AD: Non-neoplastic diseases of the tonsils and adenoids, in Paparella MM, Shumrick DA (eds):

Otolaryn-gology. Philadelphia, WB Saunders, 1980, vol 3, pp 2278-2279

22. Richardson MA, Seid AB, Cotton RT, et al: Evaluation of tonsils and adenoids in sleep apnea syndrome. Laryngoscope

1980;90:1106-1 110

23. Bortnick E: Neoplasms of the nasal cavity. Otokiryngol Gun

North Am 1973;6:801-812

24. Masing H: Rhinological problems in the newborn and nurs-lings.

mt

J Pediatr Otorhino/aryngol 1979;1:25-32

25. Batsakis JG: Tumors of the Head and Neck: Clinical and Pathological Considerations, ed 2. Baltimore, Williams & Wilkins, 1979, pp 280-288, 291-312, 341-346

26. Levey M: Hemangioma of the nasal septum.

mt

Surg

1976;61:344-349

27. Biller HF, Sessions DG, Ogura JH: Angiofibroma: A treat-ment approach. Laryngoscope 1974;84:695-706

28. Fitzpatrick DJ, Briant TDR, Berman JM: The nasopharyn-geal angiofibroma. Arch Otokzryngol 1980;106:234-236

ANNOUNCEMENT

OF THE

1984

WRITTEN

EXAMINATION

OF

THE

AMERICAN

BOARD

OF PEDIATRICS

The 1984 Written Examination of the American Board of Pediatrics will be administered on Friday, September 14 in various cities throughout the United States and Canada.

Application material for the certifying examination of the Board is available throughout the year by writing to the Board Office at the address below. The completed material of those applicants who wish to be considered for the 1984 Written Examination must be postmarked by January 31, 1984.

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1983;72;766

Pediatrics

Charles M. Myer III and Robin T. Cotton

Nasal Obstruction in the Pediatric Patient

Services

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http://pediatrics.aappublications.org/content/72/6/766

including high resolution figures, can be found at:

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1983;72;766

Pediatrics

Charles M. Myer III and Robin T. Cotton

Nasal Obstruction in the Pediatric Patient

http://pediatrics.aappublications.org/content/72/6/766

the World Wide Web at:

The online version of this article, along with updated information and services, is located on

American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

Figure

Fig 1.Bilateralatresiaplatepreventsdye fromenteringnasopharynx.
Fig 3.Surgicallyresectedcongenitalmidlinenasalmass(A) confirmedby histopathologyto be a dermoidcyst.
Fig 4.Regionpalateof nasopharyngealstenosis(A) secondaryto distortionandscarringof soft(B)andposteriorpharyngealwall(C)followingtonsillectomyandadenoidectomy.
Fig 5.Endoscopicviewof posteriorchoanademonstrat-ingedematousturbinates(A)andpurulentrhinorrhea(B)asseenwithinfectiousrhinitis.Softpalate(C)islabeledfororientation.
+5

References

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