NASAL DISORDERS

Nose provides for—(a) initial warming and humi­dification of inspired air, (b) filtration of large suspended particles (gt;6 #956;), (c) mechanical microbial clearance by forward ciliary movements in nasopharynx and (d) immunological defence by secretary IgA and lysozymes in nasal secretions.

Choanal atresia is the commonest congenital malfor­mation of the nose (1:7000), characterized by unilateral or bilateral, bony (90%) or membranous septum, between nose and pharynx. Other congenital anomalies are present in ~50% cases, including CHARGE syndrome (coloboma of eye, heart anomalies, Atresia choanae, retarded growth/renal anomalies, genital and ear anomalies).

Clinically unilateral atresia is often asymptomatic, except unilateral nasal discharge and stuffiness. However, bilateral choanal atresia present at birth with breathing difficulties and cyanosis specially during feeding, as newborns are obligatory nose breathers.

Diagnosis is suggested by: (a) failure to pass a catheter beyond the posterior nares, (b) spatula test for unilateral lesions, i.e. absence of steam vapors on affected side when a shining steel tongue depressor is kept in front of nares, and (c) lateral skull radiographs with a contrast medium instilled in the nostrils. CT/MRI studies are recommended to delineate bony anatomy before surgery. Treatment: Bilateral choanal atresia needs immediate surgery in neonatal period with perforation/dilatation of membranous lesions or transnasal resection with stenting in bony lesions, after initial stabilization with oral airway or tracheostomy. Correction of unilateral atresia may be deferred for many years.

Acute rhinitis (common cold) is the commonest infection in childhood, with ~3-8 attacks per childhood years.

Etiology: Common cold is a viral illness, predominantly caused by—(a) rhinoviruses in 1/ 3^rd cases, (b) corona­viruses, and (c) respiratory syncytial viruses.

Incidence of rhinoviral infections is higher in—(a) preschool children, (b) winter season, (c) overcrowded slums/day-care centres, (d) passive smokers and (e) air pollution due to domestic smoke, vehicular or industrial emissions.

Pathogenesis: All common cold viruses are transmitted via droplets, close physical contact and fomites. Offending virus invades upper airway epithelium leading to release of chemical mediators (nasal itching) vascular edema with exudation (rhinorrhoea/stuffiness) and bronchoconstriction (cough). Sometimes, infection may spread downwards to cause sore throat, croup or bronchiolitis.

Strain-specific immunity develops within a week, mainly involving secretary IgA, with recovery. Subse­quent infections are caused by different strains. Clinical manifestations begin after 2-5 days of incubation period with local symptoms, e.g. acute rhinorrhoea, sneezing, nasal block, conjunctival congestion, mild cough or sore throat, etc., with or without systemic symptoms, e.g. fever, headache and bodyache.

Young infants may have feeding difficulties and disturbed sleep due to nasal obstruction. Night cough is common due to post-nasal drip. Nasal discharge is initially watery, but thickens gradually due to shedding of epithelial cells and leukocytes. Purulent discharge indicates secondary infection. Course is self-limiting with recovery in 5-7 days.

Common complications include: (a) otitis media, (b) sinusitis, (c) pneumonia, (d) croup, (e) triggering of asthma.

Diagnosis is clinical and cultures or serology is rarely indicated.

Treatment is symptomatic with—(a) plenty of oral fluids,

(b) saline nasal drops to clear stuffy nose, (c) steam inhalation and (d) pharmacotherapy with antipyretics, antihistaminics and decongestants. Antibiotics do not affect the course, unless secondary infection is present.

Vitamin C and zinc, commonly claimed to be cold- preventors, are of doubtful value.

Allergic rhinitis is a common atopic disorder in children, characterized by seasonal or perennial attacks of sneezing, rhinorrhoea and nasal stuffiness.

Pathogenesis: Like other allergies, allergic rhinitis is also associated with—(a) inherent or acquired hyper­responsiveness of nasal mucosa, and (b) IgE mediated hypersensitivity on exposure to inhalant allergens, e.g. pollens, dust, danders, molds, etc.; leading to mucosal congestion, edema and excessive mucus secretion.

Clinically, allergic rhinitis may present with seasonal or perennial attacks, most intense during first 4-5 years of age. Family history of atopy is present in ~1/4^th cases.

Acute attacks present with sudden onset of sneezing, profuse watery/mucoid rhinorrhoea, nasal stuffiness and itching sensation in nose, pharynx and ears. Conjunctival redness, itching and tearing may also be present.

After recurrent attacks, child may develop: (a) certain mannerisms, e.g. frequent wrinkling, i.e. rabbit nose, or rubbing of nose, i.e. allergic salute, (b) horizontal creases over nose, i.e. Dennie's lines, (c) creases on lower eyelids, i.e. Dennie-Morgan folds, (d) periorbital puffiness or dark circles, i.e. allergic shiners, and (e) Allergic gape with continuous open-mouth breathing.

Local examination may reveal bluish or pale nasal mucosa with mucoid discharge, hypertrophic pharyngeal follicles and post-nasal drip. Recurrent episodes ma

lead to development of nasal polyps, atrophic rhinitis, sinusitis or otitis media.

Classification: Presently, AR is classified as—(a) mild intermittent, (b) mild persistent, (c) moderate to severe intermittent, and (d) moderate to severe persistent, based on the frequency of attacks as intermittent or persistent (symptoms for lt;/gt; 4 days/week for more than 4 weeks) and severity of the attack as mild or moderate-to-severe (with disturbed sleep, school performance or daily activity).

Many cases have associated complications or comor­bidities, e.g.

Diagnosis is mainly clinical, supported by: (a) family history, (b) presence of eosinophils in nasal secretions, and (c) eosinophilia with raised IgE levels.

Identification of precipitating allergen is neither easy nor necessary in all cases, though may be possible in some older children by history, in vivo skin testing or in vitro Specific IgE estimation by serum immunoassays (Ch 8.4.1). Skin tests are negative in first few years of life due to sensitization confined to nose and sinuses.

D/D includes other causes of recurrent or persistent rhinorrhea including: (a) recurrent viral infections, (b) vasomotor rhinitis, (c) rhinitis medicamentosa, (d) nasal foreign body, and (e) anatomical causes, e.g. deviated nasal septum, nasal polyps, etc.

Vasomotor rhinitis is triggered by internal events, e.g. exercise, cold/heat exposure, strong odors, while rhinitis medicamentosa is caused by over-use of topical decongestants.

Management includes treatment of acute attacks and prevention of recurrent attacks.

• Acute attacks may be treated by oral antihistamines, preferably second-generation long-acting less-sedat­ing cetirizine, fexofenadine or loratadine. Intranasal antihistamines (INAH) can be used in older children gt;6 years, though generally not preferred due to bitter trickle-down taste and somnolence. Topical deconges­tants, e.g. Xylometazoline may be used briefly for nasal obstruction but should be avoided due to rebound congestion and risk of rhinitis medicamentosa.

• Prevention of attacks needs intranasal steroids (INS) with low systemic bioavailability as sprays in minimum possible doses, e.g. mometasone or fluti­casone (50-100 #956;g#8725;nostril OD in morning). Systemic steroids are rarely required.

Leukotriene-modifyingagents (LTRA), e.g. Montelukast, have a modest effect on rhinorrhea and nasal blockage and can be used in selected cases.

Other preventive measures include: (a) avoidance of allergen exposure, e.g. dust, fumes and smokes, (b) topical mast-cell inhibitors, e.g. cromolyn sodium nasal spray on

For abbreviations, see text

long-term basis, and (c) immunotherapy for desensitization against identified allergen, though rarely useful.

A step-wise approach is recommended by ARIA (allergic rhinitis and its impact of asthma) guidelines 2019, for management of allergic rhinitis (Table 16.13).

Nasal polyps are benign pedunculated tumors of chronically inflamed mucosa, seen in-chronic sinusitis, allergic rhinitis and cystic fibrosis. These polyps often originate in middle meatus and present with persistent rhinorrhea, hyponasal speech, mouth-breathing and grape­like glistening-gray masses on rhinoscopy. Prolonged use of local decongestants and steroid spray may reduce the size of polyp, though surgery is needed in some cases.

Nasal foreign bodies, e.g. grains or peanuts, are common in toddlers, which may present immediately after lodgement or after many days with unilateral foul-smelling discharge, swelling and noisy breathing. Local trauma, aspiration and rarely tetanus are potential complications.

Easily visible foreign body may be removed by forcible blowing of nose or manually by forceps, suction or Katz catheter, if necessary after instillation of a topical decongestant to reduce the edema.

However, sharp, embedded or posteriorly located bodies need removal by ENT surgeon under rhinoscopic guidance. Blind attempts should be avoided due to the risk of pushing them further or aspiration.

Epistaxis (nose-bleed) is a common problem in childhood, especially in dry hot weather.

Etiologically, local trauma due to nose-picking or foreign body is the commonest cause of epistaxis (Table 16.14), with bleeding from Kiesselbach's plexus (Little area) in anterior septum. Epistaxis from posterior septum or during sleep may lead to mild hematemesis/melena.

TABLE 16.14: Causes of epistaxis

• Local trauma: Nose picking, foreign bodies

• Infections: Acute rhinitis/sinusitis

• Allergic rhinitis

• Vascular: Telangiectasia, varicosities

• Nasal growths: Polyps, hemangioma

• Systemic: Bleeding disorders, leukemia*

• Hypertension

*specially promyelocytic type

Management of acute epistaxis includes: (a) local pinching of nose, (b) cold compresses, and (c) forward tilting of head to avoid tricking of blood in posterior pharynx, and (d) topical decongestants, e.g. xylometazoline. Nasal packing for few hours is required in some cases.

After control of bleeding, local examination helps to identify bleeding site, which may be cauterized with 1% silver nitrate. Children with recurrent epistaxis should be evaluated for systemic causes or posterior septal mass.

16.5.2