EAR DISORDERS
External and middle ear as well as ossicles develop from first two branchial arches and grooves, while rest of the inner ear develops from otocyst.
Congenital malformations of ear include: (a) external ear abnormalities, e.g.
preauricular pits/tags or microtia, (b) external auditory canal atresia/stenosis, (c) ossicular malformations, leading to conductive deafness and (d) congenital perilymphatic fistula, leading to sensorineural deafness.Malformations of external or middle ear, though largely benign and cosmetic, are frequently associated with inner ear defects or other congenital anomalies, e.g. renal malformations or chromosomal syndromes. Hence, complete auditory and renal evaluation is necessary in all children with ear malformations, along with cosmetic or functional interventions.
Otitis externa: While external ear canal is colonized by various aerobic and anaerobic organisms, it is protected by presence of a water-repellent waxy cerumen, derived from apocrinal and sebaceous secretions and exfoliated skin.
Otitis externa is the acute or chronic inflammation of external ear canal, sometimes associated with furunculosis or eczematous lesions.
Etiology: Excessive wetness, (e.g. swimming), dryness (lack of cerumen), trauma (foreign body) or neighbouring skin infections are predisposing factors for otitis externa, usually caused by Pseudomonas, Staph. aureus, anaerobes and occasionally, Candida (Otomycosis).
Clinically, these cases present with—(a) acute otalgia that typically accentuates on pressing the tragus or moving the pinna, (b) edema, redness and thick, clumpy otorrhea in ear canal, with or without, (c) temporary conductive hearing loss. Itching is more prominent in chronic otitis externa or otomycosis, while furunculosis is an extremely painful superficial abscess.
Diagnosis rests on otoscopic examination to rule out foreign body or furunculosis.
Presence of herpetic vesicles on external auditory canal and pinna along with facial paralysis is termed Ramsay-Hunt syndrome.Management includes—(a) topical antibiotics and/ or antifungal drops, (b) oral analgesics, and (c) local anesthetic ear drops in severe painful ear. During early stages, when edema may prevent entry of topical drugs in ear canal, a cotton-wick soaked with desired topical drug may be used to facilitate drug delivery. Ear should be thoroughly cleaned with irrigation after control of acute inflammation to prevent recurrence.
Otitis media (OM), i.e. inflammation of middle ear cleft, includes a spectrum of ear-pathology, classified in order of increasing severity as: (a) acute otitis media without effusion, (b) acute otitis media with effusion, (c) chronic otitis media with effusion (OME), and (d) chronic suppurative otitis media (CSOM) with/without cholesteatoma.
Epidemiology: Nearly 2/3rd of children have at least one attack of OM by 3 years of age, with highest incidence in late infancy (6-12 months). It is more common in boys and during winter season.
Important risk factors of OM include: (i) top feeding, (ii) foreign body, (iii) passive smoking, (iv) recent measles, (v) gastroesophageal reflux, (vi) immunodeficiency disorders, and (vii) institutionalized care in orphanages, etc.
Pathogenesis: OM is more common in younger children due to: (a) relatively horizontal position of eustachian tube, preventing adequate drainage, and (b) higher incidence of nasopharyngeal infections and adenoidal hypertrophy, which block the opening of eustachian tube due to mucosal edema. Gradual absorption of air in middle ear after eustachian tube obstruction results in negative pressure gt; transudative effusion gt; secondary infection gt; rise in middle ear pressure gt; perforation of tympanic membrane.
Microbial etiology: Strept. pneumoniae (30-50%) and H. influenzae (20-30%) are two commonest pathogens in OM, followed by others, e.g.
S. aureus, Moraxella catarrhalis, E. coli, Klebsiella and Pseudomonas. OM due to mycoplasma, chlamydia, tuberculosis, viruses and anaerobic organisms is relatively rare.Clinically, acute OM presents with sudden onset of severe otalgia, otorrhoea, fever and constitutional symptoms, usually during or soon after common cold. GIT upsets is common in young infants.
Direct visualization of tympanic membrane reveals congested, opaque, bulging tympanic membrane with restricted mobility, with/without perforation and suppurative discharge. Foreign bodies should also be excluded on otoscopy.
CSOM presents with persistent ear discharge for gt; 6 weeks with non-intact tympanic membrane, broadly categorized as-(a ) Safe with simple central perforation of parse tensa or (b) Unsafe perforations involving attic and posterosuperior region with high-risk of intracranial complications and cholesteatoma
Complications include: (a) hearing loss, (b) infection of surrounding structures, e.g. labrynthitis, mastoiditis or petrositis, (c) intracranial infections, (d) tetanus, (e) cholesteatoma, and (f) facial palsy.
Diagnosis is based on otoscopy, supported by ear-swab cultures. Although tympanocentesis for fluid culture is more reliable for microbial diagnosis, it is indicated only in cases with: (a) poor therapeutic response, (b) serious or immunodeficiency illness, (c) co-existing intracranial infection.
For common causes of otalgia see Table 16.15.
TABLE 16.15: Common cause of otalgia (earache)
• Otitis media (or blocked Eustachian tubes)
• Otitis externa, i.e. furunculosis, herpes, otomycosis
• Foreign body or trauma
• Impacted cerumen (wax)
• Referred pain from teeth, temporomandibular joint, etc.
Treatment: Antibiotic therapy in OM is largely empirical, based on local drug sensitivity profile. Oral amoxicillin (40-50 mg/kg/d q8hr) for 10 days is the drug of choice in most cases. Higher doses (75-90 mg/kg/day) must be considered in populations with higher risk of resistance.
Other drugs like Coamoxiclav or second-generation cephalosporins may be used in resistant cases.Supportive therapy includes analgesics, decongestants, e.g. pseudoephedrine, and local hot fomentation. Antihistamines and steroids are not useful.
Surgical interventions, e.g. myringotomy with Tympanostomy tube placement may be needed in cases with severe AOM, CSOM or recurrent OM. These tubes usually extrude spontaneously in 6-9 months.
Recurrent OM, defined as gt; 2 episodes in 6 months or gt;3 episodes in a year, should be considered for tympanostomy tube insertion and adenoidectomy to reduce the frequency of episodes.
Mastoiditis, i.e. inflammation of mastoid air cells, is an important complication of otitis media.
Clinically, it is characterized by retroauricular pain/ tenderness, induration, redness and downward/ outward shifting of pinna with blurring of postauricular sulcus and sometimes, formation of mastoid abscess. Infection may extend intracranially to cause meningitis or brain abscess or rupture externally.
Diagnosis rests on clinical features and lateral X-ray of the skull, revealing: (a) haziness of mastoid outline, (b) loss of pneumatization, and (c) sclerosis of air-cells in chronic mastoiditis. CT scan is necessary to confirm the diagnosis and exclude intracranial extension.
Treatment depends on the severity of disease, including antibiotics (as for AOM), drainage of pus (if localized) and mastoidectomy in extensive or chronic disease.
Foreign body in ears, e.g. insects, left-over cotton buds and grains, etc., are common in all age-groups and usually present after many days with earache, discharge, tragus swelling, ringing sensation or temporary deafness. Tympanic perforation and tetanus are most important complications.
Visible foreign bodies may be removed by a sterile, wet cotton-bud or forcep, followed by instillation of topical antibiotic drops. However, long-standing bodies may be impacted or tend to move further inside on repeated attempts and need auroscopic or surgical removal by otolaryngologists.
Also see IMNCI guidelines for management of child with ear problems (Ch 29).
16.7