Paediatric otolaryngology has become a mature surgical sub-specialty in the last decade. The management of otolaryngological disorders in infants and children requires specific expertise in both otolaryngology and in the care of children. In addition, as the survival rates of small premature infants has improved, a team approach to their care has developed involving neonatologist, paediatrician, otolaryngologist, and other paediatric specialists.

An initial discussion of the nomenclature of ear infections is important. Otitis media refers to inflammation of the middle ear, without reference to pathogenesis. Acute otitis media is synonymous with suppurative or purulent otitis media, while otitis media with effusion is inflammation of the middle ear with fluid and no tympanic membrane perforation. The perforation persists for less than 3 weeks; if it lasts for 3 weeks to 3 months it is referred to as subacute, while chronic otitis media with effusion persists for longer than 3 months. Serous media or secretory otitis media are synonyms for otitis media with effusion. The term chronic otitis media indicates a perforated eardrum and should be qualified as being with or without cholesteatoma.

Otitis media is the most common illness causing a child to visit a physician. One-third of children will have had at least one episode of otitis media by the age of 1 year, two-thirds will have had at least one episode by the age of 3 years, and one-third will have had over three episodes by this age. Fluid in the middle ear frequently persists after the completion of 10 days of antibiotic treatment; however 50 per cent of treated patients still have fluid after 4 weeks, 20 per cent after 8 weeks, and 10 per cent after 12 weeks.

The pathogenesis of otitis media is primarily eustachian tube dysfunction. Children under the age of 6 years have an increased incidence of otitis media because the eustachian tube is more horizontal and shorter than in the adult. Non-pharyngeal contaminants may lead to a complex inflammatory response in the middle ear and a decrease in mucociliary transport. Functional obstruction (adenoid tissue, allergic oedema) may cause a high negative pressure in the middle ear which may result in a sterile effusion. This effusion frequently becomes secondarily infected.

Factors which appear to increase the incidence of otitis media include immunodeficiency, use of day care centres, and exposure to cigarette smoke in the home. Patients with craniofacial anomalies such as cleft palate, and those with Down's syndrome have a significantly increased incidence of otitis media.

Ear pain, irritability, increased ear pressure, and decreased hearing acuity are symptoms of acute otitis media. Fever may or may not be present in infants. The diagnosis is made on pneumatic otoscopy which reveals a full or bulging tympanic membrane, usually red but sometimes white or yellow, which moves poorly.

The microbiology of acute otitis media has been well studied. The causative organisms are Streptococus pneumoniae (previously Diplococcus pneumoniae), 29 per cent, Haemophilus influenzae (non-typable), 23 per cent; Branhamella catarrhalis (previously Neisseria catarrhalis) 8 to 15 per cent, group A &bgr;-streptococcus, 4 per cent and Staphylococcus aureus, 2 per cent. Negative cultures may represent viral infections or infections with anaerobic bacteria. Up to 30 per cent of the H. influenzae and almost all of the B. catarrhalis isolates are &bgr;-lactamase producers and resistant to ampicillin drugs. The initial treatment is most commonly amoxicillin (40 mg/kg. day in three doses for 10 days). Myringotomy and aspiration is indicated if there is no improvement in the acute symptoms and findings over 48 h. If resistant organisms are suspected, amoxicillin with clavulanic acid, cefaclor, or erythromycin/sulphonamide should be administered).

Children with recurrent acute otitis media, defined as three episodes in 6 months or five episodes in 12 months may benefit from prophylactic antibiotics for 1 to 3 months. (amoxicillin 20 mg/kg.day in a single dose or sulfroxizole 25 mg/kg twice daily).

Persistent middle ear effusion may cause more subtle symptoms and signs, such as ear fullness, hearing loss, loss of appetite, ear tugging, and malaise. Despite the absence of acute symptoms or physical findings, 25 per cent of these ears have bacteria present. The causative organisms are the same as those responsible for acute otitis media. For this reason, another trial of a different antibiotic may be useful.

The indications for insertion of a ventilation tube (grumet) are listed in Table 1 578. Such tubes are usually inserted under general anaesthesia and are left in place for 6 to 12 months. Potential complications are persistent tympanic membrane perforation, cholesteatoma formation, tympanosclerosis, tube otorrhoea and of course, recurrence of otitis media when the tube has extruded.

Adenoidectomy may reduce the incidence of recurrences of acute otitis media and otitis media with effusion, particularly in patients in whom ventilation tube treatment has not been successful and in whom symptoms of upper airway obstruction such as snoring or mouth breathing are apparent. The size of the adenoid may not be as important as lymphatic stasis and pooling of infection in and around the eustachian tube resulting from the presence of the adenoid tissue.

Frequent otorrhoea in the presence of a tympanic membrane perforation usually indicates either mucosal infection or ingrowth of a benign skin-lined white sac-like cyst (cholesteatoma). Most acquired cholesteatomas develop from a perforation or a deep retraction pocket containing squamous epithelial debris, especially in the superior part of the tympanic membrane (confined to the attic area of the middle ear). Surgical removal of the skin lining, reconstruction of the ossicular chain, and reconstruction of the tympanic membrane with a fascia graft is required, and mastoidectomy is often necessary to rid the middle ear/mastoid of the disease.

Congenital cholesteatoma (epithelial rest behind intact tympanic membrane) is less common than acquired cholesteatoma. These most commonly arise in the anterior superior quadrant of the middle ear space and require surgical removal.

External otitis is active inflammation of the ear canal and sometimes the pinna; moisture in the ear canal is the usual cause. Swimming, showers, washing the hair, and even humid climates may predispose the ear canal to infection. Local trauma with a fingernail or cotton swabs allow bacterial entry through the skin of the ear canal. Localized conditions such as eczema and psoriasis may also alter the canal skin and predispose to infection. Staphylococcus aureus is the most common cause of acute external otitis while Pseudomonas and fungi (Aspergillus and Candida) may cause a chronic infection.

Symptoms range from mild itching to fullness and throbbing pain. Movement of the ear canal on opening the jaw or moving the pinna exacerbates the pain and allows otitis externa to be distinguished from otitis media. The external auditory canal is frequently oedematous and may be filled with foul-smelling debris.

Treatment begins with elimination of water from the ear canal and warnings against the introduction of swabs and other instruments. Prophylactic use of alcohol/vinegar drops in a 1:1 mixture after swimming is helpful if the tympanic membrane is intact. Careful, gentle cleaning of the ear canal with suction or a loop under microscopic guidance is essential. Prompt administration of topical antibiotic or steroid drops and avoidance of water are the main principles of treatment. Occasionally placement of a wick of cotton (or commercially prepared wick) may be required for 2 to 4 days to help resolve ear canal swelling and allow drops to enter the canal. Broad-spectrum antibiotics are rarely used unless there is inflammation of the pinna, cervical adenopathy, or fever.

Hearing loss in children is usually first noticed by parents or teachers. In infants, a subtle lack of response to sudden noises and unusual behaviour indicate hearing loss. Delayed speech and language development may be the initial signs in a toddler or older child. A unilateral hearing loss may go undetected for years as communication skills may initially appear to be only slightly affected.

Hearing loss is classed as mild (30–40 dB hearing level), moderate (40–50 dB), severe (50–70 dB), and profound (>70 dB). Loss of greater than 60 dB is usually sensorineural or mixed (conductive and sensorineural). Hearing loss may be stable, progressive, or fluctuating, depending on the aetiology. The specific tone frequencies lost are important; the result determines the effect on speech and language development. Conductive hearing loss, the most common hearing problem in children, is usually due to middle ear fluid or infection. Congenital malformation of the ossicular chain, trauma, or ossicular erosion by chronic infection may also result in a conductive hearing loss. Impaction of cerumen rarely causes a significant conductive hearing loss.

Sensorineural hearing loss is usually congenital and may be genetic or acquired in utero following infection of the fetus by agents such as rubella virus, Toxoplasma, and cytomegalovirus, exposure to drugs, or metabolic disorders. Genetic causes are usually inherited in an autosomal recessive manner and may also produce malformations in other systems. Infantile or childhood meningitis remains a significant cause of acquired sensorineural hearing loss.

The pinna is exposed to trauma due to its location on the lateral surface of the skull. Blunt trauma may cause ecchymosis of the soft tissue or a haematoma, causing interruption of the blood supply. Cartilage damage may result and a significant cosmetic deformity may occur (cauliflower ear). Participants in contact sports should wear protective headgear to prevent auricular damage. Haematomas or seromas should be drained before cartilage damage occurs. Frostbite of the pinna may follow exposure to extreme temperatures. The ear should be warmed rapidly with moist cotton soaked in saline at 37 to 40°C. Excessive manipulation should be avoided.

Foreign bodies in the ear canal are commonly encountered in children. Swelling of vegetable matter causes infection, odour, drainage, and pain. Plastic or metal objects and rocks may be found on routine examination in patients with minimal symptoms. The shape and size of the foreign body directs how it should be removed; irregular edges may be grasped with alligator forceps, while an ear loop or wax curette or right angle hook inserted behind a small, round object may roll it out. A foreign body located near the tympanic membrane may be dislodged by gentle irrigation with water at body temperature or moved to a location in the ear canal where it can be reached with a loop or forceps. Insects may be killed with mineral oil or alcohol (provided the eardrum is intact) and then removed by forceps or irrigation. Antibiotic or steroid ear drops applied after foreign body removal hasten healing of the canal if abrasion or irritation has occurred.

Traumatic perforation of the tympanic membrane may be caused by a penetrating foreign body (including cotton applicators), a slap to the side of the head, or activity such as diving or water skiing. Most small or moderate perforations will heal spontaneously in 6 to 8 weeks, if infection is prevented, water contamination is avoided, and the tympanic membrane edges are not folded into the middle ear. Folded edges should be teased up under microscopal control to promote healing and to avoid inward migration of squamous epithelium (cholesteatoma). Barotrauma during flying or scuba diving rarely results in traumatic perforation: haemotympanum (blood in the middle ear) is more common. the latter may become infected, in which case antibiotics are required. Myringotomy is recommended if the blood or fluid persists for longer than 3 weeks.

All of the above injuries may also cause traumatic ossicular chain disruption and/or perilymph fistula.

Blunt trauma to the head may fracture the temporal bone. Transverse fractures usually result from occipito or frontal blows and may cause haemotympanum, sensorineural hearing loss, vertigo, and facial nerve paralysis. Longitudinal fractures may occur from more lateral blows and may disrupt the tympanic membrane, ossicles, and the external ear canal. These are less likely to cause sensorineural hearing loss and facial nerve paralysis. Computerized tomography of the temporal bones may help to delineate the presence and location of the fracture.

Clear rhinorrhoea or otorrhoea after temporal bone fracture suggests a CSF leak. Repair using a neurosurgical otological or combined approach may be necessary. Delayed facial nerve paralysis due to swelling may be treated in the same way as Bell's palsy, but immediate paralysis requires surgical exploration, decompression, or repair.

Sudden hearing loss and/or vertigo following straining, lifting, or strenuous exercise may be due to acute perilymph fistula formation. Exploration and fat or fascia patching of the leak at the oval and round windows is required if spontaneous healing does not occur.

Acute bacterial sinusitis is usually secondary to viral upper respiratory infection, anatomical deformity of the nasal passages, or allergic rhinitis. The causative organisms are similar to those of otitis media (Streptococcus pneumoniae, Haemophilus influenzae, &bgr;- haemolytic streptococci and Branhamella catarrhalis); choice of antibiotic is also similar therefore. Most acute episodes are treated for 21 days. Physical examination discloses purulent rhinorrhoea in the middle meatus. Nasal congestion and cough are commonly associated with sinusitis in children, while halitosis, fever, facial pressure and pain, which are common in adults, are less common in paediatric patients. If sinusitis is persistent, or unresponsive to treatment, or recurrent radiographs may show air/fluid levels with acute mucosal thickening or total opacification (Fig. 3) 2222. Reasons underlying failure of antibiotic therapy or recurrence can be diagnosed by culture of a specimen obtained by antral puncture, which is more informative than a swab of the nose or nasopharynx. Puncture is performed through the inferior meatus and usually requires general anaesthesia in children. Careful attention to the high positioning of the floor of the maxillary sinus in children as well as the location of tooth buds is important. Frontal sinus trephination through a small medial eyebrow incision may occasionally be required.

Complications of sinusitis include orbital and intracranial spread of infection. Periorbital (preseptal) cellulitis causes oedema of the upper eyelid and is treated with intravenous antibiotics active against Staphylococcus and H. influenzae. Orbital cellulitis causes chemosis, proptosis, and limitation of eye movement; aggressive intravenous antibiotics and topical nasal decongestant drops usually resolve these symptoms. Reduced visual acuity requires immediate drainage of sinuses and orbit. Orbital abscess is treated in a similar fashion, but is more likely to result in permanent visual loss. Cavernous sinus thrombus is extremely rare and manifests itself with bilateral signs of orbital abscess. This grave condition is treated with intravenous antibiotics, anticoagulants, and drainage of the infected sinus. Mortality rate is 15 per cent.

Intracranial complications of sinusitis include meningitis, and epidural, subdural, and brain abscesses; these are becoming less common as ability to diagnose disease rapidly and to administer aggressive therapy improves.

The nose is a passageway for air, which it also warms, filters, and humidifies. Nasal obstruction in children may result from anatomical deformity, an obstructive mass, or an alteration in the physiological function of the nose. Epistaxis, anosmia, hyponasal speech, and rhinorrhoea may accompany obstructive symptoms. Intranasal examination with a head mirror or headlight and nasal speculum is essential, and a flexible fibreoptic endoscope may also provide valuable information. Intranasal examinations are usually enhanced by the use of topical intranasal vasoconstrictive agents, such as 0.25 per cent Neo-Synephrine. Paranasal sinus radiographs, CT scan, or MRI scan may be required.

Congenital nasal obstruction may be secondary to choanal atresia due to the failure of the nasobuccal membrane to rupture in the fourth embryonic week. This condition occurs in 1/8000 births, is usually unilateral, and is more common in females. Most cases (90 per cent) are due to bony rather than membranous atresia.

Since the infant is an obligate nasal breather for the first weeks to months of life, bilateral choanal atresia may cause severe early respiratory distress. The diagnosis is confirmed by failure to pass nasal catheters (No. 6 and No. 8 French); CT examination will further define the nature of obstruction (bony versus membranous; thin versus thick). Keeping the infant's mouth open with a McGovern nipple or an oral airway may allow mouth breathing to be learned (Fig. 4) 2223. Feeding by orogastric tube may be necessary. If the infant learns to mouth breathe and gains weight, transpalatal repair is usually undertaken at 6 to 12 months of age, although earlier intervention is frequently necessary. Transnasal rupture of a membranous bilateral atresia may be performed early in life if required. Although the use of stents is controversial, stenting for 4 to 6 weeks with endotracheal tube modifications is generally used in combination with either intranasal or transpalatal repair. Over 50 per cent of affected infants have other congenital deformities, and this condition may be part of the CHARGE association (Coloboma, Head defects, Atresia of the choana, Retarded growth and development, GU abnormalities, and External ear deformities).

Anterior or posterior nasal stenosis may occur and cause similar but milder symptoms of atresia. Initial conservative management, with brief use of nasal topical decongestants, frequent saline drops and suctioning may be sufficient until growth occurs. Surgical repair is rarely necessary.

Dermoid cysts are congenital epithelium-lined rests at lines of embryonic fusions. The nasal midline, between the nose and orbit, and lateral supraorbital ridge are usual sites of these cysts. They may present with external pits at the nasal dorsum. Intracranial connections are possible, but uncommon.

Encephaloceles and gliomas are epithelial and/or glial extensions of the central nervous system into the nasal and facial area. Encephaloceles, which may connect with the central nervous system and contain CSF, are usually pulsatile and enlarge with crying. Gliomas, unlike encephaloceles, have no central nervous system connection. CT and MRI scans are helpful in evaluating the possibility of intracranial extension in these cases. Excision is frequently carried out for safety and cosmetic reasons, using a combined neurosurgical and otolaryngological approach.

Intranasal foreign bodies may cause obstructive symptoms and, if undetected, will cause unilateral malodorous, purulent rhinorrhoea. The differential diagnoses of unilateral foul-smelling nasal drainage include foreign body, unilateral choanal atresia, and unilateral intranasal tumour. Suction and a topical nasal decongestant helps to establish the diagnosis. When a foreign body is seen, removal with suction, blunt hook, or forceps may be possible. However, removal under general anaesthesia is often required in order to avoid dislodging the foreign body posteriorly into the airway.

Epistaxis is relatively common in childhood, and most episodes are secondary to inflammation or trauma. A history of bleeding, easy bruising, trauma, or possible associated illness (such as leukaemia) must be obtained. The anterior septum (Kiesselbach's triangle or Little's area) is the most common site because of the presence of a plexus of vessels. Careful examination and use of a topical nasal decongestant is important. Single finger pressure to squeeze the nostrils together usually controls active bleeding. Cauterization with silver nitrate, packing with absorbable collagen or gelatin, or even anterior packing with antibiotic-impregnated gauze may be necessary. Posterior packing with lamb's wool or a Foley catheter with the balloon inflated is very rarely needed in children. If this is the case, admission is required while the pack is in place. Subsequent rebleeding can be prevented by the use of nasal saline drops, humidification, and topical vaseline applications. Nasal septal deviation, sinusitis, tumour (angiofibroma), foreign body, and blood dyscrasia are uncommon causes of childhood epistaxis, but deserve consideration if epistaxis is persistent.

When exterior and posterior nasopharyngeal packing fails to control haemorrhage, ligation of the internal maxillary artery may save the day. Ligation of the external carotid artery is sometimes practised in this circumstance but is not generally effective.

Newborns may acquire a septal deviation during birth, indicated by a tilted columella, tip deviation, and alar asymmetry. If the septum is dislocated from the vomer groove immediate closed reduction with an intranasal instrument such as an elevator should be attempted. If dislocation has not occurred, spontaneous correction is likely to occur over 6 to 8 weeks.

Trauma to the nose in a child may cause a haematoma of the septum. This must be diagnosed and drained intranasally with needle aspiration or incision and drainage to prevent loss of cartilage support and resultant saddle nose deformity. Closed (or open) reduction of nasal fractures should wait until swelling has resolved over 5 to 7 days, but should be undertaken before fibrous healing makes reduction impossible. Closed reduction is optimal within 7 days following trauma. Unreduced nasal fractures may produce significant functional and cosmetic abnormalities which may require septorhinoplasty during later years.

Most throat infections are viral and therefore require no antibiotics. Throat cultures are necessary for the diagnosis of bacterial infections. Pharyngitis or tonsillitis due to &bgr;-haemolytic streptococci is treated with penicillin for 10 days; erythromycin or cefaclor may be used for those allergic to penicillin.

Peritonsillar abscess or quinsy is localization of pus in the space between the tonsil capsule and the superior constrictor muscles of the pharynx. The tonsil and soft palate bulge medially and the uvula deviates away from the abscess. Intravenous administration of penicillin, with excision and drainage, is required. Many otolaryngologists recommend tonsillectomy 6 weeks later.

Retropharyngeal abscess may develop from suppurative adenitis of retropharyngeal nodes, and is best seen on a lateral neck film taken in inspiration and neck extension. Parapharyngeal abscess from the parapharyngeal lymph nodes is best seen as pharyngeal fullness and neck swelling. Intravenous antibiotics with incision and drainage are required for the treatment of both of these conditions.

The indications for adenotonsillectomy relate primarily to the frequency and severity of infection and the extent of airway obstruction. Most otolaryngologists recommend adenotonsillectomy if tonsillitis occurs 4 to 6 times per year or if airway obstruction occurs secondary to tonsillar and adenoidal hypertrophy, presenting as mouth-breathing, snoring, restless sleep, or full sleep apnoea syndrome. Midface hypoplasia, dental malocclusion, and severe orthodontic problems have been described secondary to prolonged mouth-breathing. Snoring and sleep disturbance can be assessed informally from a cassette tape recording of a patient's breathing during sleep. A formal sleep laboratory study is helpful in quantifying the degree and severity of sleep apnoea. Enuresis may occur in the child with sleep disturbances secondary to upper airway obstruction and severe obstruction may lead to cor pulmonale.

A common abnormality is a short lingual frenulum (ankyloglossia) or ‘tongue-tie’. There is usually no need for surgical correction unless eating, speech, or dental development is affected. In this case surgical release with simple incision or Z-plasty may be done. Care must be taken to avoid damage to the sublingual salivary ducts.

A bifid uvula may be associated with a submucous cleft palate or absence or weakness or the midline palate aponeurosis, the notch in the posterior edge of the hard palate. Adenoidectomy is contraindicated in these children to avoid development of significant velopharyngeal incompetency, resulting in nasal regurgitation and hypernasal speech. Infants with cleft palate may require a special large-opening nipple to enable feeding. Cleft lip usually is repaired at the age of 3 to 4 months and palate repair is performed at 12 to 18 months. Most children with cleft palate develop otitis media with effusion at an early age and require ventilation tube insertion as early as 3 to 6 months of age, in conjunction with plastic surgery.

Infection in the salivary gland (sialoadenitis) may be viral or bacterial. Viral mumps is uncommon: immunity produced by administration of live mumps virus vaccine is widespread. Bacterial infection presents with signs and symptoms similar to cervical adenitis-fever, swelling, pain, and tenderness. Massage of the affected parotid or submandibular gland will produce pus at the duct opening. Intravenous antibiotics, heat, massage of the gland, increased fluid intake, and sialogogues such as lemon drops are helpful. Recurrent or chronic sialoadenitis may be caused by ductal stricture, stones, immunodeficiency, or autoimmune disorders. If continued painful swelling occurs, drainage or gland excision may be necessary.

While salivary gland tumours are uncommon in children, the parotid gland is most commonly affected. The most common parotid neoplasm in children is the benign haemangioma, which may be detected early in life and is frequently associated with cutaneous lesions. Most enlarge over 6 to 12 months and then undergo spontaneous regression over several years. Systemic corticosteroids may help the tumour to regress. Lymphatic malformations may present as a soft, painless, compressible mass in the parotid region. They rarely resolve spontaneously and may cause significant airway obstruction if cervical or supraglottic involvement is prominent.

Excluding hamartomatous malformations, over 50 per cent of salivary gland tumours in children are malignant. CT scan may be helpful and fine needle aspiration, where available, may help as an initial procedure. Local pain, rapid growth, facial paralysis, and systemic changes are suggestive of malignancy. Malignant parotid tumours are treated with total parotidectomy; the facial nerve is sacrificed only if the tumour involves the nerve. Neck dissection is recommended for palpable positive regional nodes. Chemotherapy and radiotherapy may be helpful in high-grade malignancy or when total excision is not possible. Submandibular tumours are more likely to be malignant than are those in the parotid.

Ingestion of caustic substances by young children is usually accidental, but may be the result of intentional child abuse. Teenagers may attempt suicide in this manner. Drooling and dysphagia are the most common presenting symptoms. Physical examination may reveal obvious injury; however the lack of oral burns does not rule out oesophageal injury. Oesophagoscopy should be performed within 48 h of the ingestion but carried out only to the level of the first burn.

The classification of burns is shown in Table 3 580. Grade I burns are limited to superficial mucosa and will not result in scar formation; Grade II burns penetrate the mucosa and may lead to strictures. Steroids appear to help these injuries. Grade III burns, penetrate deeper into the mucosa and should not be treated with steroids for fear of oesophageal penetration. A barium swallow is obtained at 3 weeks and gentle periodic dilatation is started if stricture formation has begun.

A foreign body ingested by a child may lodge in the oesophagus, most commonly at the cricopharyngeal inlet (velopharyngeal), aortic knob, and the oesophagogastric junction. Small, round objects usually pass through the gastrointestinal tract. Endoscopic removal under general anaesthesia with airway intubation is the safest way to retrieve an oesophageal foreign body. Foreign bodies in the oesophagus frequently cause airway symptoms with stridor, croupy cough, and wheezing due to tracheal compression through the adjacent wall.

Hoarseness is best defined as an alteration of the normal voice; this may range from a weak, breathy cry in an infant with vocal cord paralysis to a hoarse, scratchy voice in an adolescent due to voice abuse at an athletic event. Oedema and inflammation due to upper respiratory tract infection is the most common cause and will resolve as the infection improves. If hoarseness persists beyond resolution of the acute illness, evaluation is necessary.

Vocal cord nodules begin as polyp-like oedema at the junction of the anterior one-third and middle one-third of the true vocal cords and are secondary to vocal cord abuse or poor voice habits. Indirect (mirror) laryngoscopy or flexible fibreoptic scope examination usually confirms the diagnosis. Referral for speech therapy is made in children over the age of 8 when they can begin to comply with instruction. Direct laryngoscopy and removal of nodules with cup forceps or CO&sub2; laser is indicated if a 6- to 12-month trial of speech therapy fails, or if fibrous nodules develop. Vocal abuse must be corrected or surgical removal will help only temporarily.

Chronic cough and throat clearing in a child with allergy and chronic sinusitis may cause vocal cord oedema and thickening. The basic cause must be controlled. Other causes of hoarseness include vocal cord paralysis, congenital laryngeal malformation (e.g. web, cysts), laryngeal papilloma, submucosal cleft palate, and gastro-oesophageal reflux. Trauma from endotracheal intubation may cause development of a granuloma on the vocal cord or arytenoid area.

Stridor is an audible sound from the airway indicating turbulent airflow due to partial obstruction. The level of obstruction determines the quality and phase of respiration of the stridor (Table 4) 581. Nasal or nasopharyngeal obstruction causes snoring or snorting sounds on inspiration. Supraglottic (epiglottis, aryepiglottic folds, false vocal cords) obstruction causes inspiratory stridor, while lower (distal trachea, bronchi, and bronchiolus) obstruction causes expiratory stridor or wheezing. The subglottic area and immediate upper trachea display a biphasic (inspiratory and expiratory) stridor when obstruction is present.

A careful history is mandatory including onset, fluctuation, possible presence of a foreign body, and any factor that alters the stridor, such as position change, feeding, or treatment. Physical examination is vital but should be limited if stridor is acute, progressive, or if severe obstruction has occurred or is imminent. Radiographic studies should only be requested in the non-urgent case; these should include anterior, posterior, and lateral chest and neck films. Fluoroscopy allows the dynamic effects of respiration of the airway to be studied and may be helpful, especially if the child is unable to co-operate for inspiratory and expiratory films. Barium swallow examination can rule out vascular ring, gastro-oesophageal reflux, tracheo-oesophageal fistula, and neuromuscular swallowing problems. Flexible fibreoptic examination of the airway may provide information on glottic and supraglottic conditions, but this technique should be used with caution if a foreign body or progressive obstruction is expected. Direct laryngoscopy, bronchoscopy, and oesophagoscopy are the definitive procedures, and should be performed under general anaesthesia with spontaneous ventilation in the operating room. Careful planning and co-operation with the anaesthesiologist is essential so that the airway can be shared safely during the examination.

Epiglottitis (supraglottis) is acute inflammatory swelling of the supraglottic larynx, including the epiglottis, aryepiglottic folds, and false vocal cords, usually caused by Haemophilus influenzae type B. The most common age is 2 to 6 years, and patients present with rapid acute onset of fever, throat pain, drooling, and airway distress with inspiratory stridor. Retractions may occur late in the process as more shallow, rapid breathing causes less supraglottic collapse with inspiration. A careful look at the throat with a tongue depressor may be difficult, and this is recommended only if symptoms are mild and intubation equipment and personnel are available. Lateral neck radiographs will demonstrate an enlarged epiglottis, but should not be obtained in severely ill children (Fig. 5) 2224. A team approach has been shown to decrease mortality associated with this diagnosis; otolaryngologist, anaesthesiologist, paediatrician, and emergency room, operating room, and paediatric intensive care unit staff should be present. The examination is undertaken in the operating room under general anaesthesia and shows a large, red, swollen epiglottis; the airway below the vocal cords is usually normal. The initial oral endotracheal tube is changed to a nasal tube and meticulously secured. Blood cultures and surface culture swabs are usually positive for H. influenzae. Concomitant extralaryngeal H. influenzae infection, including pneumonia and meningitis, may also occur. After 36 to 48 h in the paediatric intensive care unit an air leak is usually noted around the endotracheal tube and the child is extubated. The initial antibiotic of choice is ampicillin/chloramphenicol or cefotoxine, pending the results of culture and antibiotic sensitivity of the blood samples. Oral ampicillin or amoxicillin treatment should be continued for 10 to 14 days unless resistance is shown. With the increased availability of the new H. Influenzae type B vaccine, administered at 15 to 18 months, acute epiglottitis has become less frequent or may appear in younger children.

Croup (laryngotracheobronchitis) usually occurs in patients under 2 years old, and is usually due to parainfluenza virus infection. The barking cough and biphasic stridor is characteristic. Onset is gradual with general symptoms of upper respiratory tract infection. Significant obstruction rarely develops, although some episodes can be severe. Radiographs show typical anterior, posterior, and lateral narrowing of the subglottic space (Fig. 6) 2225. Mild cases are managed with cool mist and increased fluid intake. If racemic adrenaline is needed, hospital admission is recommended to observe the patient for rebound. Corticosteroid administration is recommended if the condition worsens to avoid the need for an artificial airway. If required, intubation with a smaller than calculated endotracheal tube for 3 to 5 days may be acceptable, although some clinicians prefer tracheostomy. Antibiotics are used only if the condition follows a prolonged course or if intubation is required.

Bacterial tracheitis is fairly common and is heralded by a history characteristic of a viral illness with a sudden rapid deterioration over 8 to 10 h. The patient has thick secretions, high fever, and tracheal crust formation which often is seen on radiographs as density in the tracheal air column with scalloping of the tracheal margins. Fifty per cent of cases are due to S. aureus. Bronchoscopy to establish the diagnosis and to meticulously suction the desquamated mucosa with crust cleaning, heavy mist, and antistaphylococcal antibiotics are the mainstay of treatment (Table 5) 582.

Laryngomalacia is the most common cause of stridor in the infant. It is thought to be caused by soft, collapsible supraglottic laryngeal structures, although there are many theories concerning its aetiology. At laryngoscopy, redundant arytenoids and a floppy, omega-shaped epiglottis are drawn into the larynx on inspiration, resulting in a high-pitched inspiratory stridor. Laryngomalacia usually begins shortly after birth, and increases when the baby is active, agitated, feeding, or lying supine. When the child is relaxed and prone, stridor is decreased or absent. Laryngoscopy and bronchoscopy should be undertaken in children who fail to thrive, or who suffer from cyanotic spells, apnoea, progressive worsening, or who fail to improve by the age of 9 to 12 months. Atypical stridor may indicate a second problem: 10 to 15 per cent of infants with stridor have a second abnormality. Rarely intubation or tracheostomy may be necessary; CO&sub2; laser division of the aryepiglottic folds to reduce the tissue in folding with inspiration may be attempted to avoid the need for tracheostomy.

Vocal cord paralysis is the next most common cause of neonatal stridor. In neonates this may be due to neck stretching during delivery, and usually spontaneously resolves. In older children, chest and skull radiographs and metabolic studies including blood sugars and thyroid function studies, are required. Unilateral vocal cord paralysis causes early hoarseness with breathy, weak cry and possibly aspiration. Arytenoid dislocation from intubation trauma must be ruled out as the arytenoid may be repositioned more easily when an early diagnosis is made. Bilateral vocal cord paralysis causes severe airway obstruction but a near-normal voice. Prompt intervention with intubation or tracheostomy is usually required. Bilateral vocal cord paralysis is usually due to central nervous system problems. In children with the Arnold-Chiari malformation, a ventriculoperitoneal shunt procedure and posterior fossa decompression may correct the vocal cord paralysis and avoid the need for a tracheostomy. Cardiac anomalies may be present, especially in those with left unilateral vocal cord paralysis. Other causes are metabolic (diabetes, thyroid), lead poisoning, trauma from neck or cardiac surgery, central vascular lines, and cervical chest or mediastinal masses.

Congenital subglottic stenosis may cause early stridor or recurrent croup-like episodes in infancy. The stridor is biphasic and may be associated with a barking cough if inflammatory swelling occurs during the course of an upper respiratory tract infection. Failure to pass a 3.5 mm bronchoscope (outer diameter) through the subglottis of a full-term newborn, is suggestive of subglottic stenosis. Mild to moderate stenosis (up to 50 per cent compromise) may respond to conservative management since growth alone may resolve the difficulty. Tracheostomy, dilatation, CO&sub2; laser resection and open laryngotracheal reconstruction may be required in more severe cases.

Acquired subglottic stenosis in neonates, especially the premature, is more likely to be due to prolonged intubation than to congenital causes. Treatment is required for all but the mildest cases. Most cases present as a failed attempt at intubation after the infant has been weaned from the ventilator and the primary need for intubation has resolved. Most reconstruction techniques involve an anterior costal cartilage graft, with or without stenting of the grafted area.

Subglottic haemangioma may also present as recurrent croup. Fifty per cent of patients with subglottic haemangiomas have other cutaneous haemangiomas. Anterior, posterior and lateral neck radiographs show asymmetrical subglottic swelling. There may be mild stridor (biphasic) between ‘croup’ episodes. This usually becomes obvious at the age of 3 to 6 months and progresses for 1 to 2 years, while the haemangioma increases in size. The typical appearance at laryngoscopy is a smooth posterolateral swelling with a bluish tint. Patients with large haemangiomas usually require tracheotomy to maintain an adequate airway. They frequently show spontaneous involution by the age of 3 to 4 years. Small haemangiomas may cause only mild symptoms and intervention is not required. Staged segmental CO&sub2; laser excision may be used to avoid tracheostomy.

Laryngeal webs and stenosis are the result of failure of the larynx to recanalize during embryonic development. Most webs are anterior at the vocal cord level, and they are an early cause of hoarseness and stridor. Congenital cysts are usually supraglottic in the vallecula and aryepiglottic folds and cause inspiratory stridor. Endoscopic removal of webs and cysts with microinstruments or CO&sub2; laser is usually possible.

Laryngotracheal clefts are uncommon and represent a form of high tracheo-oesophageal fistula. These clefts cause early stridor, hoarseness, aspiration, and choking. Early correction is necessary, except for very small shallow clefts; a midline or lateral neck approach is usually required.

Vascular anomalies such as anomalous innominate artery, right aortic arch, double aortic arch, anomalous right subclavian artery, and pulmonary artery sling may cause respiratory symptoms including stridor, wheezing, coughing, pneumonia, and feeding problems. Chest radiographs and barium swallow are helpful, but often the diagnosis is made at endoscopy. MRI or CT scan of the chest may confirm the diagnosis; however an arteriogram is rarely necessary. Aortoplexy or correction of the vessel abnormalities may be necessary.

Foreign bodies that lodge in the larynx may be rapidly fatal unless coughing clears the material from the laryngeal inlet. If there is absolutely no air passage and no phonation, a Heimlich manoeuvre or suspending the child by its feet and back slaps to dislodge the foreign body may be lifesaving. Emergency cricothyroid space tracheostomy is rarely successful in small children. Foreign bodies in the tracheobronchial tree cause symptoms related to the specific area. Vegetable matter may swell and fragment, causing early symptoms, but obstruction due to plastic and metal objects may be asymptomatic for a prolonged period of time. Unilateral wheezing, air trapping on the affected side, and mediastinal shift away from the affected side on expiration is diagnostic of partial airway obstruction (Fig. 8) 2227. Fluoroscopy is usually necessary to show the phases of respiration in a small child, and direct laryngoscopy and bronchoscopy are required. An oesophageal foreign body should not be overlooked as a cause of airway obstruction due to tracheal compression through the party wall which is particularly compliant in children.

Tracheostomy is usually performed in a child for prolonged assisted ventilation secondary to neurological or cardiac problems, failure to extubate a premature infant with bronchopulmonary dysplasia, pulmonary secretion toilet in a neurologically disabled patient, and, occasionally, for congenital or acquired airway obstruction. Ideally the procedure should be undertaken over an endotracheal tube or bronchoscope in the operating room. A vertical skin incision assures that the surgeon remains in the midline, and the cosmetic result is quite acceptable after the stoma has matured around the tube and formed a circular scar. Traction sutures of 2–0 silk are used laterally along the vertical tracheal incision through tracheal rings two and three. These traction sutures make reinsertion of the tube easier if accidental extubation occurs in the early postoperative period. The smallest tube that will allow adequate suction and air exchange is used if the child is not on a ventilator; for those on a ventilator, a larger tube with a good seal is necessary. The tracheostomy tube is changed after the first 7 days and then every 7 to 14 days.

Cervical masses in children require systematic evaluation and management. A thorough history, complete examination of ear, nose, throat, head, and neck are necessary. Radiographic studies, including sinus films and neck CT are often helpful. Skin tests for tuberculosis are also applied. When antibiotic therapy does not cause adenopathy to resolve or if diagnostic studies are inconclusive, an excisional biopsy is recommended.

Inflamed lymph nodes account for the majority of neck masses in children. The nodes are tender and usually multiple. Cervical node infections may break down and form an abscess, indicated by fluctuance and shiny red changes of the overlying skin, although chronic infection may result in multiple firm nodes that are non-tender and without skin changes. Cat-scratch fever, atypical mycobacteria, and toxoplasmosis may require biopsy for diagnosis. Staphylococcus aureus is the most common cause of an abscess and is treated with intravenous antibiotics. When fluctuance develops, needle aspiration may hasten recovery and allow an organism to be cultured. Larger and more persistent abscesses require incision and drainage in the operating room. CT helps to locate and define the abscess. Parapharyngeal abscesses lying between the pharyngeal constrictor muscles and the vascular compartment, cause a stiff neck and fever, and the child is usually septicaemic. Dysphagia is common. Incision and drainage through the neck is required, followed by intravenous administration of antibiotics active against staphylococci. Retropharyngeal abscess may develop in a similar fashion, between the retropharyngeal fascia and prevertebral fascia. This space connects the base of the skull to the mediastinum and infection may spread up or down if not controlled. Lateral neck radiographs taken in full extension and inspiration show a bulge of the space, sometimes with air formation. Intravenous antibiotics and intraoral (and sometimes external neck) incision and drainage are required.

Congenital masses are most common after inflammatory masses of the neck. Persistence of the embryonic branchial cleft causes branchial cleft anomalies of the head and neck. If the lateral cleft is obliterated, a cyst may develop; this may connect to the pharynx if the medial cleft persists and to the neck if the lateral cleft persists. A sinus connects from cyst to pharynx or cyst to skin surface, while a fistula connects pharynx and skin surface. Lymphatic tissue and cartilage rests may lie in the cyst or tract. A first cleft cyst and tract may present as a cyst in a position posterior and inferior to the ear canal and connect to the skin of the ear canal and into the parotid gland and facial nerve area. The second cleft anomaly is the most common, presenting as a cystic mass and/or a sinus opening in the neck anterior to the sternocleidomastoid muscle. Collections of epithelial debris and infection may take years to develop; this accounts for the variable age at which the congenital anomaly presents. An infection may be the first indication of a problem. If a tract persists, it passes from the cyst between the internal and external carotid arteries, superior to the hypoglossal nerve (XII) and inferior to the glossopharyngeal nerve, (IX) to terminate in the tonsillar fossa. If a tract extends up and down from the cyst, multiple step-ladder neck incisions may be required for its removal. Third and fourth cleft cysts are more unusual.

Thyroglossal duct cyst is an epithelial lined cyst persisting along the course of descent of the thyroid gland from the foramen caecum at the base of tongue to the lower midline of the neck. The most common site is at or below the hyoid bone, where it usually moves up and down with swallowing and tongue extension and retraction. Infection and collection of mucoid material cause the cyst to present as an enlarging or inflamed mass. There is no outward extension through the skin unless previous aspiration, incision and drainage, surgery, or spontaneous rupture has occurred. Differential diagnoses include cervical node, dermoid, and neoplasm. A thyroid scan should be performed to ensure that the mass is not the sole functioning thyroid tissue. Surgical excision involves removal of the central segment of the hyoid bone with the specimen (Sistrunk procedure). Extension to the base of tongue often requires a core of tongue tissue to be removed in order to achieve tract excision.

This tumour is an organizing haematoma which arises as a result of perinatal trauma. It presents as a mass in the sternocleidomastoid muscle and torticollis. Fibrosis develops in the haematoma, typically causing symptoms at the age of 3 to 6 weeks. Conservative treatment with heat and passive motion usually resolves the problem. Surgery to resect the fibrosis and lengthen the muscle is rarely necessary.

Haemangioma of the head and neck (including the parotid gland) is the most common head and neck neoplasm in children. Rapid growth for 12 to 18 months is usually followed by slow resolution over 1 to 2 years. Observation is the preferred management strategy, unless airway obstruction, haemorrhage, high output cardiac failure, or platelet trapping occurs. Lymphatic malformations (cystic hygroma) consist of multiple cystic spaces filled with lymph. A large transilluminating neck mass is the most common presentation. Progressive enlargement usually occurs; a rapid increase in size may be due to haemorrhage or infection. Airway compromise may occur. Spontaneous resolution is rare and surgical excision is recommended for all but the smallest of lesions. Surgical procedures may be staged for large lesions, the first procedure being performed at 9 to 12 months of age. Respiratory or feeding problems in a neonate may require insertion of a tracheostomy or gastrostomy tube.

Fortunately, malignant tumours are not common in childhood. The most common malignant neoplasm in children is lymphoma, Hodgkin's and non-Hodgkin's lymphoma being roughly equally common. Multiple firm, rubbery nodes are present, and excisional biopsy is required for diagnosis. Radiation therapy is used to treat localized disease, with the addition of chemotherapy for systemic or diffuse disease. Well-differentiated Hodgkin's lymphoma has a better prognosis than non-Hodgkin's lymphoma.

Rhabdomyosarcoma is the most common soft tissue head and neck malignancy in childhood, the diagnosis being suggested by a rapidly growing painless neck mass. The diagnosis is confirmed by biopsy, and treatment consists of excision of as much of the tumour mass as is reasonably possible, followed by radiation therapy and chemotherapy.

Squamous cell carcinoma of the nasopharynx, melanoma, neuroblastoma, and thyroid malignancy may initially present as cervical adenopathy.

Ear

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Nose and paranasal sinuses

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Oral cavity and oropharynx

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Larynx and trachea

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Neck

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