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 Table of Contents  
Year : 2012  |  Volume : 18  |  Issue : 4  |  Page : 200-207

Clinical and audiological evaluation of hearing impaired children

Department of ENT and HNS, Government Medical College, Srinagar, Jammu and Kashmir, India

Date of Web Publication19-Dec-2012

Correspondence Address:
Zafarullah Beigh
90 Feet Road, Bachapora, Srinagar, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-7749.104799

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Daily activities, interpersonal relationship, employment, and general well being; among such skills, communication skills are essential to a successful life for all individuals. Such skills affect education, adequate hearing acuity is of paramount importance and acts as a prerequisite in the overall personality development of an individual. Hearing impairment at any age has serious effects on the day to day life of an individual and he/she feels handicapped socially, emotionally, and scholastically. A child stuck with this malady is a back bencher in the class, excommunicative, and absent-minded. This study was conducted in order to find out various causes of hearing impairment in children and to study role of various audiological and radiological tests in finding the cause of impaired hearing in children. Aims and Objectives: To assess the possible etiological causes of hearing impairment in children. Study role of various audiological tests in finding the cause of impaired hearing in children. Study Design: Prospective study. Materials and Methods: This study was conducted in the Department of ENT and HNS of government medical college Srinagar. A total of 150 children of age range 0-14 years visited our ENT Department with complaints of impaired hearing, but only 70 children who met the inclusion criteria of impaired hearing and defective/delayed speech were selected for this study. Results of initial evaluation by means of comprehensive clinical history and followed by proper thorough systemic physical examination from head to toe was performed. These hearing impaired children were subjected to various subjective and objective tests; pure tone audiometry and behavioral observation audiometry were performed for subjective tests and impedance audiometry, Oto-acoustic emissions (OAE), and brainstem evoked response audiometry (BERA) were performed for objective tests. Results: Possible etiological cause on the basis of history were birth anoxia (2.85%), premature (5.71%), low birth weight (4.28%), hyperbilirubinemia (4.28%), and consanguinity (42.86%). Possible cause revealed after proper systemic examination includes 2.85% children with craniofacial abnormalities, 2.85% children with Down's syndrome, and 1.42% with Usher's syndrome. OAE revealed 70% bilateral REFER and 30% bilateral PASS. Impedance audiometric results were mostly Type A tympanogram. Pure tone audiometric results were mostly on profound hearing loss (86.69%). BERA findings were mostly on profound hearing loss (85.79%). Conclusion: In this study large vestibular aqueduct (LVAQ) is most common cause of abnormality detected in hearing impaired children.

Keywords: Audiology, Children, Hearing impaired

How to cite this article:
Beigh Z, Malik MA, ul Islam M, Yousuf A, Pampori RA. Clinical and audiological evaluation of hearing impaired children. Indian J Otol 2012;18:200-7

How to cite this URL:
Beigh Z, Malik MA, ul Islam M, Yousuf A, Pampori RA. Clinical and audiological evaluation of hearing impaired children. Indian J Otol [serial online] 2012 [cited 2022 Jun 25];18:200-7. Available from: https://www.indianjotol.org/text.asp?2012/18/4/200/104799

  Introduction Top

There is convincing evidence to suggest that for the optimal development of speech and language, the auditory pathway must be stimulated from a very early age to allow it and its higher centers to mature properly. [1]

At present, considerable research is directed toward improving the early detection of deafness, which is the most important task faced by otorhinolaryngologists.

A deaf person is defined as those in whom the sense of hearing is nonfunctional for ordinary purpose of life or hearing loss of >95 dB (profound) or total deafness and who do not understand/hear sound at all even with amplified speech and fail to develop speech. These children have often been termed as deaf-mute or deaf and dumb. However, these children have no defect in their speech producing apparatus. The main defect is deafness. They have never heard speech and therefore do not develop it.

In lesser degrees of hearing loss, speech does develop but is defective. The period from birth to 3 years of life is crucial for the development of speech and language, therefore, there is need for early identification and assessment of hearing loss and early rehabilitation in infants and in children. [1]

It was observed that children whose hearing loss was observed and managed before 6 months of age had higher scores of vocabulary, better expressive and comprehensive language skills than those diagnosed and managed after 6 months of age emphasizing the importance of early identification and treatment. [2]

Deafness may be mild, moderate, severe, or profound. [2] Deafness is classified into three groups: [3],[4]

  1. Conductive deafness: This occurs when the sound conducting mechanism of the ear is defective. The lesion could be anywhere from the external auditory canal to the footplate of stapes.
  2. Sensorineural deafness: This type of deafness is due to abnormality in the cochlea, auditory nerve, neural pathway, or their central connections with auditory cortex.
  3. Mixed deafness: It denotes that both conductive and sensorineural abnormality is present in the deaf person.
Hearing loss in a child may develop from causes before birth (prenatal), during birth (perinatal), or thereafter (postnatal).

Hearing impairment is the most common form of sensory disorder in humans. Yet relative to our knowledge of sensory transduction in vision, taste, and smell, the molecular components of mechanotransduction of sound responsible for hearing are poorly understood. Further, the critical components involved in differentiation and function of inner ear remain largely unidentified. [3]

History taking constitutes an essential part of the evaluation process. In the neonatal period, concern is related to family history, prenatal infection, perinatal events, and physical stigmata. In the infantile period, attention is turned to postnatal events, including prenatal concerns about hearing, speech, language, and developmental delay. [5]

All systems of the body have been associated with sensorineural hearing loss (SNHL). Physical findings can occur in isolation or a part of a syndrome. Hence, a thorough systemic physical examination from head to toe can help uncover cases of syndromic hearing impairments. Physical findings associated with syndromic hearing loss should be referred for evaluation to a multispeciality clinic. [5]

Radiographic imaging of temporal bone can identify inner ear malformation that may be responsible for hearing impairment. In evaluating children with unexplained SNHL radiological studies such as computed tomography (CT) and magnetic resonance imaging (MRI) have made it possible to identify a specific cause of auditory impairment. In general, CT is the first line recommended imaging modality for SNHL. [6]

The prevalence of permanent, moderate-to-severe SNHL is estimated between 1 and 2 per 1000 live births. [7],[8]

This disorder has a variety of causes and can be generally classified according to genetic and nongenetic etiologies. Approximately 15-30% of hereditary hearing impairment involves other organ systems and occurs as a syndrome. [9]

  Materials and Methods Top

The present prospective study was conducted in the Postgraduate Department of Otorhinolaryngology, Head and Neck Surgery of Government Medical College, Srinagar on OPD-attending population, of Kashmiri children, with hearing impairment and defective/delayed speech.

Inclusion criteria

  1. Children ≤ 14 years of age.
  2. All children with SNHL and delayed/defective speech
Exclusion criteria

  1. Age >14 years.
  2. Children with conductive hearing loss or with history of ear discharge as in chronic suppurative otitis media or acute suppurative otitis media (CSOM or ASOM).
  3. Children with conductive hearing loss due to otitis media with effusion [OME].
  4. Children with impaired hearing but with normal speech.
  5. Children with defective speech but with normal hearing.
When parents brought their child to the OPD, the following important history was extracted from parents as per proforma:

Antenatal history

  1. Was there any ill-health of mother during her pregnancy?
  2. Was there any drug intake during her pregnancy?
  3. Was there any history suggestive of syphilis, maternal rubella, or other specific fever during pregnancy?
Natal history

  1. Where was child born: in hospital or at home?
  2. Did the child cry at birth or not?
  3. Was there any history suggestive of birth asphyxia?
Postnatal history

  1. Is there any history suggestive of admission in neonatal ICU (NICU) of their child?
  2. Is there any history suggestive of neonatal jaundice?
  3. Is there any history suggestive of neonatal septicemia for which neonate had received drugs?
Family history

  1. Is there any history of deafness in the family of either parent?
  2. Are the parents related to each other - consanguineous marriage?
  3. How many children are there in the family and are there any deaf children among them?
Past history of child's health

What illness has the child suffered till date, like history suggestive of meningitis in childhood; history suggestive of exposure of ototoxic drugs or history of head injury or history of any systemic disease?


  1. At what age, if at all, did speech develop, did the child babble normally? If so, did the child babble for a short time and then stop?
  2. If the child is suspected of being partially deaf, is the tone defective or is there a difficulty in pronouncing consonants?


  1. Does the mother communicate with child by voice or by signs?
  2. Can the child hear when spoken to from another room?
  3. What is the greatest distance at which the child can hear when spoken to?
  4. Does he react to the noise of a motor car, the wireless, or the door bell?
Age of onset

At what age was deafness first suspected?

State of development

  1. What standard of education has the child reached?
  2. At what age were the normal milestones reached, for example, sitting up, learning to crawl?
Physical examination

As per proforma protocol:

  1. Audiological Tests.
  2. Behavioral observation audiometry (in children ≤3 years of age).
  3. Pure tone audiometry (PTA) (in children >3 years of age.
  4. Impedance audiometry.
  5. OAE.
  6. Brainstem evoked response audiometry (BERA).
After all these investigations, the child was thoroughly assessed to determine the etiological factors associated with hearing impairment and defective speech.

This study was conducted in the Department of Otorhinolaryngology and Head and Neck Surgery, SMHS Hospital Government Medical College, Srinagar (J and K). This study was completed over a period of 2 years. This study included children aged 0-14 years. A total of 150 children with impaired hearing visited our ENT OPD but only 70 children were selected for this study who fulfilled the inclusion criteria.

[Table 1] shows the distribution of patients with hearing impairment in different age groups and percentage of age group. Maximum number of patients are seen in the age group of 1-5 years and minimum <1 year.
Table 1: Age distribution (n=70)

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[Table 2] shows sex distribution of hearing impaired children; shows males outnumber females and equal number of males and females in age group of <1 year.
Table 2: Sex distribution (n=70)

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[Table 3] shows sex ratio of hearing impaired children; sex ratio was maximum in age group 5-10 and minimum in age group 10-15. [Table 4] shows district wise distribution of hearing impaired children with maximum no. of patients from Srinagar district. [Table 5] shows maximum number of hearing impaired children is seen in rural areas.
Table 3: Male/Female ratio

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Table 4: District wise distribution (n=70)

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Table 5: Rural/Urban distribution

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[Table 6] shows that 42.86% children with hearing impairment were born out of consanguineous marriage.
Table 6: Marriage type

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[Table 7] shows that 12.85% children with positive family history of hearing impairement. [Table 8] shows 92.8% children were non syndromic and 7.14% were syndromic. [Table 9] shows cranio facial abnormality and Down's syndrome in two children each while as Usher's syndrome was seen in one childasphyxia. [Table 10] shows possible etiological cause identified on the basis of history, prematurity in 5.71% children, hyperbilirubinemia in 4.28%, low birth weight in 4.28% and birth asphyxia in 2.85%. [Table 11] shows results of behavioural observation audiometry in children less then 3 years of age mild hearing loss was present in 20% children and moderate to profound loss in 80% children. [Table 12] shows result of pure tone audiometry done in children >3 years of age. Profound hearing loss was present in 86% of children and severe hearing loss in 14% of children. [Table 13] shows result of impedance audiometery. Type A curve was obtained in maximum [38%] no. of children. [Table 14] shows acoustic Reflex was absent in all 70 children. [Table 15] shows result of oto acoustic Emission, Reffer was present in 70% and pass in 30% of children. [Table 16] shows BERA findings, profound hearing loss was present in 85% of children and severe hearing loss in 11% of children, 2.8% of children had moderate hearing loss.
Table 7: Family history of hearing impairment

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Table 8: Syndromic versus nonsyndromic

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Table 9: Type of syndromic abnormality

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Table 10: Possible etiological causes identifi ed on the basis of history

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Table 11: Behavioural observation audiometry in children <3 years of age (n=20)

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Table 12: Pure tone audiometry in children >3 years of age (n=50)

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Table 13: Impedance audiometry (n=70)

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Table 14: Acoustic refl ex measurements (n=70)

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Table 15: Oto-acoustic emission

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Table 16: BERA fi ndings (n=70)

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  Discussion Top

The study entitled "Study of Clinical, Audiological and Radiological Evaluation of Hearing Impaired Children" was performed in Government Medical College and associated Hospital over a period of 2 years. A total of 150 children aged 0-14 years with impaired hearing visited the Department of ENT and HNS of SMHS Hospital Government Medical College, Srinagar in 2 years. Out of the 150 children, only 70 children with both hearing impairment and delayed/defective speech were selected for this study.

Early identification and appropriate treatment of hearing loss in children is critical for normal development. Although universal newborn hearing screening programs are leading to increased diagnosis of hearing loss; but identifying the etiology in children can be challenging. Hence, a thorough investigation of the child is needed in respect of clinical, audiological, imaging, and referral to other specialists. These evaluations often result in extensive and expensive assessments in trying to identify the cause of hearing impairment. Hearing loss may exist as part of syndrome and its identification may allow for anticipation of associated complications and appropriate management

These children were brought by their parents to OPD with complaints of delayed speech and language development or impaired hearing and defective speech or inconsistent response to sound. Initial evaluation in identifying children with hearing loss was started with comprehensive clinical history. A thorough pregnancy and postnatal history was investigated to identify risk factors associated with impaired hearing.

In this study, there were four (5.71%) children who were born premature, three (4.28%) children were low birth weight (<1500 g), two (2.85%) children were born with birth anoxia; out of which 1 child had features of hypoxic encephalopathy on MRI scan. Three (4.28%) children had hyperbilirubenemia, but they all had normal CT scan. This study results are in corroboration with Mafong et al., [6] who in their series of 114 patients had 8% children born premature, 5% with low birth weight, 3% with ototoxic medication, and 3% with abnormal Apgar score. This study results also closely match the results of the study by Dunmade et al. [10] However, other study in this regard were made by Madden et al., [11] who investigated the clinical features of 22 students with auditory neuropathy and found history of hyperbilirubenemia in 11 (50%) patients, prematurity in 10 (45%), exposure to ototoxic drugs in 9 (41%), family history of hearing loss in 8 (36%), neonatal ventilator dependence in 8 (36%), and cerebral palsy in 2 (9%).

A careful family history helps to screen for hereditary hearing impairment. Nine (12.85%) children were from those families who have either paternal or maternal history of hearing loss.

A careful history of consanguinity should be inquired. In this study, 30 (42.86%) children belonged to families with consanguineous marriage and 40 (57.14%) were with nonconsanguineous marriage. This study is in consistent with Reddy et al. [12] study, who in a series of 1076 children found that 41.73% were products of consanguineous marriage and 58.27% were born of nonconsanguineous marriage. However, other studies in this regard are: Zakzouk et al., [13] who reported 50% consanguinity in hearing loss among 6421 subjects and Al-Ghazali LI et al., [14] who revealed 74% consanguinity in a genetic etiological survey of severe childhood deafness in united arab emirates (UAE).

A thorough systematic physical examination from head to toe can help uncover cases of syndromic hearing impairment. Physical findings associated with syndromic hearing loss should be referred for evaluation to a multispeciality clinic. In this study there were two (2.85%) children with craniofacial abnormalities; one with Treacher Collin syndrome and other with Pierre-Robin syndrome. Further in this study, there were also three other syndromic children; two (2.85%) with Down's syndrome and one (1.42%) with Usher syndrome.

In this study, there were two (2.85%) children, one with bilateral and the other with unilateral ear deformities in the form of microtia. This study nearly matches with the Derek et al. [6] study, who in their study found 5% children with craniofacial abnormalities, 5% children with ear deformities, and 5% children with musculoskeletal anomalies. However, Ohlms et al. [15] in their study found 49 (43%) children with head and neck abnormalities: 23 (20%) had defined craniofacial anomalies, whereas 26 (23%) had other abnormal physical findings including aural atresia in 7.

After detailed history and systemic examination, these children were selected for various audiological tests; but before proceeding for these tests, an otoscopic examination was performed to rule out any impacted wax that would hamper the audiological tests.

Behavioral observation audiometry

It is a method of observing the motor responses of young children to test the sound intensities to determine the hearing threshold. It is a subjective test.

For all practical purposes, a very accurate assessment of hearing is difficult in young children less than or equal to three years of age. The smaller the child, the more difficult is the hearing assessment. The test process used for assessment of a child's hearing is dependent upon the responses that a child is capable of making at that particular age.

  1. Neonates and infants <6 months of age: Auropalpebral reflexes, arousal reflex, startle reflex.
  2. 6-18 months of age: Distraction test and free field audiometry
  3. 6-36 months of age: Visual reinforcement audiometry
  4. 2-5 years of age: Performance testing.
In our study there were 20 children below 3 years of age in whom behavioral observation audiometry (BOA) was performed; this study findings were 4 (20%) children with mild hearing loss and 16 (80%) children with moderate to profound hearing loss. In the remaining 50 children who were above 3 years of age, PTA was performed; this study findings were 43 (86%) children with profound hearing loss and 7 (14%) children with severe hearing loss. Our results match with the results of Kartas et al., [16] who in their series of 218 patients, 86.69% had profound hearing loss and 10.3% had severe hearing loss on PTA.

Impedance audiometry

It has been one of the major advancements in the fields of otology and neurotology in recent times. It provides information about the nature and anatomical site of a lesion. It helps in objective differentiation between conductive and SNHL, helps in differential diagnosis of conductive deafness, helps in measurement of middle ear pressure and evaluation of Eustachian tube dysfunction, helps in differential diagnosis of sensorineural deafness, that is, whether a lesion is cochlear or retrocochlear; helps in identification of site of lesion in facial palsy and certain brainstem pathologies. Impedance audiometry is very useful for objective assessment of the approximate hearing threshold in patients where subjective audiometry is difficult.

In this study, impedance audiometric results were Type A right 26 (37.14%); Type A left 27 (38.57%); Type B right 7 (10.02%); Type B left 5 (7.14%); Type C right 3 (4.28%); Type C left 2 (2.85%). This study by and large matches with the Khayria et al. [17] study, who in their cohort of 150 hearing impaired children found type A right (37.162%), type A left (38.175%), type B right (11.148%), type B left (7.432%), type C right (4.054%), and type C left (2.027%).

No acoustic reflex was elicited with either ipsilateral or contralateral stimulation at maximum stimulation output in any patient.

Oto-acoustic emissions

Oto-acoustic emissions (OAE) can be defined as the audiofrequency energy that originates in and is released from the cochlea, transmitted through the ossicular chain and tympanic membrane, and measured in the external auditory meatus. They can occur either spontaneously or in response to acoustic stimulation. They are produced by healthy outer hair cells of cochlea. It is generally agreed that the presence of OAE indicates that the preneural cochlear receptor mechanism together with middle ear system, responds to sound in a normal way. In other words, OAEs are seen as an inevitable byproduct of the processes that are essential to hearing.

There are two broad classes of OAE, spontaneous OAE (SOAEs), and evoked OAE (EOAEs). SOAEs are continuous narrow band signals emitted by human ear in absence of sound stimulation.

EOAEs occur either during or immediately following acoustic stimulation. There are several types of EOAEs and they are classified according to evoking stimulus. The two major types we find that are used mostly in clinical setting are Transient evoked otoacoustic emissions (TEOAE) (also known as click evoked OAEs) and Distortion product otoacoustic emissions [DPOAE]. TEOAEs are recorded in response to a click or tone pip. DPOAEs are measured in response to two tones presented to the ear.

DPOAE are indeed able to test the micro mechanical properties of outer hair cells in frequency specific regions.

DPOAEs are believed to be a rapid, objective, reliable, and repeatable measure of the physiological integrity of the outer hair cells [OHC] of cochlea. These phenomenons can be recorded in almost all normal ears and are known to be reduced or absent in ears with hearing loss.

Then the results of OAE done on all children irrespetive of age were recorded; although knowing that this test is mostly used for screening purposes only in infants. The study results were: in 49 (70%) it was bilateral REFER and in the remaining 21 (30%) it was bilateral PASS.

Brainstem evoked response audiometry

It is the most popular objective test and is noninvasive. It helps in detection and quantification of deafness in difficult to test patients like infants and mentally retarded children. It objectively determines nature of deafness whether sensory or neural. It helps in identification of site of lesion in retro-cochlear pathologies, study of central auditory disorders, and study of maturity of central nervous system.

When a sound reaches the cochlea, it is converted into an electrical impulse and passes from the cochlea to the auditory cortex through the following pathway:

Spiral ganglion in the cochlea → ventral and dorsal cochlear nuclei in brainstem → superior olivary complex in mid brain → lateral lemniscus in the midbrain → inferior colliculus in the midbrain → medial geniculate body in the thalamus, and auditory cortex, that is, the portion of cerebral cortex that processes auditory signals. The BERA test evaluates the structural integrity of this pathway from spiral ganglion to the level of the lateral lemniscus.

Classification of BERA results is based on appearance of wave V on particular stimulus. [18]

Then all these children were subjected to BERA after proper preparation of head and sedation (Promethazine).

The study findings were 60 (85.79%) children with profound hearing loss; 8 (11.42%) with severe hearing loss, and 2 (2.85%) with moderate hearing loss. The study results match with Kartas et al., [16] who in their series of 218 patients, found on BERA testing that 88.07% had profound hearing loss and 11.41% had severe hearing loss. Loh et al. [18] estimated hearing responses of high risk children using BERA and found severe to profound hearing loss of 70%, moderate to moderately severe of 18%, and normal to mild of 12%.

Effect of degree of hearing impairment on speech development

Bilateral SNHL has been associated with significant language delays and disorders when comparing language development of children with educationally significant hearing loss with those who have normal hearing.

The advantage of early identification with intervention prior to 6 months of age was seen for each degree of hearing loss: mild, moderate, moderate-severe, severe, and profound. In the study of Yoshinaga-Itano et al., [19] there was a lack of relationship between degree of hearing loss (mild through profound bilateral SNHL) and language development among early identified children (identification and intervention prior to 6 months of age) between the ages of birth and 36 months of age; but a significant differences in the language development of children with mild through profound bilateral SNHL were found among later identified children (identification and intervention after 6 months of age). Children with mild through profound hearing loss, identified prior to 6 months of age and receiving intervention within 2 months of diagnosis, were indistinguishable by language quotients (language age divided by chronological age multiplied by hundred). Early identified children had significantly higher cognitive development than later identified children. The early identified children with both normal cognitive development and low cognitive ability had significantly higher language developmental quotients than later identified children. The children with cognitive delays ranged from developmental quotients (DQ) from low 20s to the high 70s. Children with normal cognitive development who were early identified had language DQ of 90.

Language development assessed both general receptive and expressive language abilities as measured by the comprehension-conceptual and expressive language subsets of the Minnesota Child Development Inventory (MCDI).

In seven patients, cochlear implantation was done and among them, the youngest was 2 years of age and oldest was 14 years of age. The youngest one developed bi-syllable words like muma, papa, which was observed 4 months postimplant. Others are on proper follow up with the speech pathologist of our department.

In summary, early identification of hearing loss, which is followed by immediate and appropriate intervention service results in better language, speech, and social-emotional development when compared with children with later-identified hearing loss, even when followed by immediate and appropriate intervention services.

  Conclusions Top

A total of 150 children with age group of 0-14 years visited the Department of ENT and HNS of SMHS Hospital Government Medical College, Srinagar in 2 years.

  1. Out of the 150 children, only 70 children with both hearing impairment and delayed speech were selected for this study.
  2. Highest number of patients were seen in the age group of 1-5 years.
  3. The patients studied had male sex preponderance and overall male: female ratio was 1.06:1.
  4. The highest number of patients belonged to the district Srinagar and rural: urban ratio was 2.8:1.
  5. Nearly 42.86% children were products of consanguineous marriage.
  6. Among 70 patients, 5 were syndromic and the rest were nonsyndromic children.
  7. Two children with craniofacial anomaly (one with Treacher Collin and other with Pierre-Robin). Two children with Down's syndrome and one with Usher's syndrome
  8. Majority of the patients (>82%) showed profound hearing loss on audiological testing.
  9. Most common tympanogram was type A (38.57%) in these hearing impaired children.
  10. Acoustic reflex was not elicited with either ipsilateral or contralateral stimulation.
  11. OAE finding was mostly REFER in 70% of hearing impaired children.
  12. Early identification of hearing loss, which is followed by immediate and appropriate intervention service results in better language, speech, and social-emotional development when compared with children with later-identified hearing loss, even when followed by immediate and appropriate intervention services.

  References Top

1.Pickett BP, Ahlstrom K. Clinical evaluation of the hearing impaired infant. Otolaryngol Clin North Am 1999;10:1019-35.  Back to cited text no. 1
2.Yoshinga-Itano C, Sedey AL, Coulter DK, Mehl AL. Language of early and later identified children. Pediatrics 1998;102:1161-71.  Back to cited text no. 2
3.Mhatre AN, Lalwani AK. Molecular genetics of deafness. Otolaryngol Clin North Am 1996;29:421-35.  Back to cited text no. 3
4.Lowe LH, Vezina LG. SNHL in children. Radiographics 1997;17:1079-93.  Back to cited text no. 4
5.Chan KH. SNHL in children. Otolaryngol Clin North Am 1994;27:473-86.  Back to cited text no. 5
6.Mafong DD, Shin EJ, Lalwani AK. Use of laboratory evaluation and radiological imaging in the diagnostic evaluation of children with SNHL. Laryngoscope 2002;112:1-7.  Back to cited text no. 6
7.Brookhouser P. SNHL in children. Pediatr Clin North Am 1996;43:1195-216.  Back to cited text no. 7
8.Mehl AL, Thomson V. New born hearing screening the great omission. Pediatrics 1998;101:e4.  Back to cited text no. 8
9.Cohen MM, Gorlin RJ. Epidemiology, etiology and genetic patterns. Hereditary hearing loss and its syndromes. New York: Oxford University Press; 1995. p. 9-21.  Back to cited text no. 9
10.Dunmade AD, Segun-Busari S, Olajide TG, Ologe FE. Profound sensorineural hearing loss in Nigerian children: Any shift in etiology? J Deaf Stud Deaf Educ 2007;12:112-8.  Back to cited text no. 10
11.Madden C, Rutter M, Hilber L. Clinical and audiological features in auditory neuropathy. Arch Otolaryngol Head Neck Surg 2002;128:1026-30.  Back to cited text no. 11
12.Reddy MVV, Hema Bindu L, Reddy PP, Usha Rani P. Role of consanguinity in congenital neuro-sensory deafness. Kamla Raj 2006. Int J Hum Genet 2006;6:357-8.  Back to cited text no. 12
13.Zakzouk S. Consanguinity and hearing impairment in developed countries: A custom to be discouraged. J Laryngol Otol 2002;116:811-6.  Back to cited text no. 13
14.Al-Ghazali LI. A genetic aetiological survey of severe childhood deafness in UAE. J Trop Pediatr 1998;44:157-60.  Back to cited text no. 14
15.Ohlms LA, Chen AY, Stewart MG, Franklin DJ. Establishing the etiology of childhood hearing loss. Otolaryngol Head Neck Surg 1996;120:159-63.  Back to cited text no. 15
16.Kartas E, Kanlikama M, Mumbuc S. Auditory functions in children at school for the deaf. J Natl Med Assoc 2006;98:204-10.  Back to cited text no. 16
17.Khayria A, Al-Abduljawad. Survey of deaf children using individual hearing AID. Bahrain Med Bull 2003;25:74-6.  Back to cited text no. 17
18.Loh KE, Yiap KH. Objective assessment of hearing loss in children using the auditory brainstem response. Singapore Med J 1984;25:278-86.  Back to cited text no. 18
19.Yoshinaga Itano C. Benefits of early intervention for children with hearing loss. Otolaryngol Clin North Am 1999;32:1089-102.  Back to cited text no. 19


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12], [Table 13], [Table 14], [Table 15], [Table 16]

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