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Summary Table

Category	Details
Risk Factors	Prenatal: family history of hearing loss, low birth weight (<2500 g), ototoxic drugs during pregnancy (aminoglycosides, antimalarials, loop diuretics, salicylates), intrauterine infections (TORCH + Zika), craniofacial malformations (microtia, ear canal atresia, cleft lip/palate, white forelock, microphthalmia, congenital microcephaly/hydrocephalus, temporal bone abnormalities). Perinatal: aminoglycoside use >5 days, hypoxic-ischemic encephalopathy/asphyxia, APGAR 0-4 at 1 min or 0-6 at 5 min, NICU stay >5 days, mechanical ventilation >5 days, hyperbilirubinemia requiring exchange transfusion, ECMO.
Etiology	50% genetic (70% nonsyndromic, 30% syndromic). Nonsyndromic: autosomal recessive 80% (GJB2/Connexin-26 mutation accounts for >50%), autosomal dominant 15%, X-linked 1%. Syndromic: Waardenburg, Pendred, Usher, Jervell and Lange-Nielsen, Alport, Treacher Collins, BOR syndrome. Nongenetic: congenital CMV (most common nongenetic cause), rubella, syphilis, herpes, toxoplasmosis.
Patient Presentation	Newborn or infant who fails newborn hearing screening (OAE or AABR refer). Older infant/toddler: absent startle reflex to loud sounds, delayed babbling, no response to name, delayed speech and language milestones. Parents may report that the child "ignores" voices or responds only to visual cues.
Classic Physical Exam	May be entirely normal in isolated nonsyndromic SNHL. Look for syndromic features: white forelock/heterochromatic irides (Waardenburg), goiter (Pendred), retinitis pigmentosa (Usher), preauricular pits/branchial fistulae (BOR), microtia/atresia, craniofacial anomalies.
Key Diagnostic Results	Screening: OAE (tests outer hair cell function; refer threshold ~30-35 dB HL) and AABR (tests cochlear-to-brainstem integrity; refer threshold ~40-45 dB HL). Confirmatory: Diagnostic BERA with tone burst (gold standard for threshold estimation in infants <6 months), ASSR, OAE, tympanometry (high-frequency 1000 Hz probe for age <6 months), acoustic reflexes, behavioral audiometry (VRA from 6 months, conditioned play audiometry from 24 months). Imaging: MRI of temporal bone (inner ear, cochlear nerve, brain). Genetic: GJB2/Connexin-26 mutation testing. Others: urine/saliva CMV PCR, ECG (rule out Jervell and Lange-Nielsen).
Management	Follows the EHDI 1-3-6 principle (screen by 1 month, diagnose by 3 months, intervene by 6 months). Hearing aid (ABD) fitting by 4 months for mild to severe loss. Cochlear implant for bilateral severe-to-profound SNHL (>70 dB) unresponsive to ABD trial, ideally before 12 months of age. Speech-language habilitation including Auditory Verbal Therapy (AVT) should begin immediately after device fitting.
Keywords	"Failed newborn hearing screen," "absent OAE," "AABR refer," "speech delay," "no response to loud sounds," "white forelock," "family history of childhood deafness," "NICU stay >5 days," "exchange transfusion," "congenital CMV."

1. Pathophysiology

Congenital SNHL arises from dysfunction at two possible sites along the auditory pathway: the cochlea (sensory) or the auditory nerve and brainstem pathways (neural).

In the cochlea, normal hearing depends on the mechanoelectric transduction performed by inner hair cells, which convert sound-wave vibrations into electrical impulses. Outer hair cells serve as cochlear amplifiers that sharpen frequency tuning and enhance sensitivity. When outer hair cells are damaged or absent, the cochlea loses its ability to amplify low-intensity sounds, producing a sensorineural threshold shift. This is the basis of most congenital SNHL cases.

The single most common genetic cause is a mutation in GJB2 (Connexin-26), which encodes a gap junction protein critical for potassium recycling in the cochlea. During transduction, potassium ions flow into the hair cells from the endolymph. After stimulation, these ions must be recycled back into the endolymph via supporting cells connected by gap junctions. A defective Connexin-26 disrupts this recycling pathway, leading to progressive potassium accumulation and hair cell death. This mutation follows autosomal recessive inheritance, which explains why most affected children have no family history of deafness, a point that test-writers exploit.

In nongenetic causes, congenital CMV is the leading culprit. The virus infects the stria vascularis and the organ of Corti, causing inflammatory damage to both the endolymphatic ion transport machinery and the hair cells themselves. CMV-related hearing loss can be progressive or fluctuating, meaning a child who passes the initial newborn screen may still develop hearing loss later, an important concept for follow-up surveillance.

A distinct subtype is Auditory Neuropathy Spectrum Disorder (ANSD), where the outer hair cells are intact (OAE is present/normal) but neural transmission is abnormal (AABR is refer/absent). ANSD is strongly associated with hyperbilirubinemia requiring exchange transfusion and aminoglycoside exposure in the NICU population. The pathology lies at the synapse between inner hair cells and the auditory nerve, or within the nerve itself.

Understanding these mechanisms is critical because they directly determine which screening test will catch which pathology. OAE tests outer hair cells only, so it will miss ANSD. AABR tests the full pathway from cochlea to brainstem, so it can detect ANSD but may miss mild cochlear loss below its threshold of 40-45 dB HL.

2. Classification and Clinical Manifestation

WHO Classification of Hearing Loss Severity

Degree	Threshold (Children)	Clinical Impact
Mild	26-40 dB HL	Difficulty hearing soft speech; may miss consonant sounds; subtle speech delay
Moderate	31-60 dB HL (children)	Cannot follow normal conversational speech without amplification; noticeable language delay
Severe	61-80 dB HL	Can hear only loud shouting at close range; marked speech/language impairment without intervention
Profound	>81 dB HL	No useful hearing for speech; reliance on visual or tactile communication without cochlear implant

Etiologic Classification

Category	Proportion	Examples
Genetic Nonsyndromic	~35% of all cases	GJB2 (Connexin-26) autosomal recessive, GJB6 (Connexin-30), mitochondrial mutations
Genetic Syndromic	~15% of all cases	Waardenburg (pigmentary anomalies), Pendred (goiter + enlarged vestibular aqueduct), Usher (retinitis pigmentosa), Jervell and Lange-Nielsen (prolonged QT), Alport (nephritis), BOR (branchial anomalies + renal anomalies), Treacher Collins (mandibulofacial dysostosis)
Nongenetic	~25-30%	Congenital CMV (most common nongenetic cause), rubella, syphilis, toxoplasmosis, herpes, Zika
Idiopathic	~20-25%	No identifiable cause

Laterality and Configuration

Type	Description
Bilateral symmetric	Both ears equally affected; most common presentation in genetic causes
Bilateral asymmetric	Both ears affected, different severities; consider CMV, progressive etiologies
Unilateral	One ear affected; risk for speech delay and academic difficulty still present
Progressive/fluctuating	May pass initial screening; develops or worsens later (CMV, enlarged vestibular aqueduct)

Auditory Neuropathy Spectrum Disorder (ANSD)

Feature	Details
Pathology	Intact outer hair cells, abnormal neural conduction (inner hair cell synapse or auditory nerve)
OAE result	Present/Normal
AABR/ABR result	Absent or severely abnormal
Cochlear microphonic	Present on BERA, follows stimulus polarity reversal (hallmark finding)
Risk factors	Hyperbilirubinemia requiring exchange transfusion, prematurity, NICU stay, aminoglycosides
Management implication	ABD trial mandatory before CI candidacy; some cases show improvement by 18 months

3. Diagnostic Workup

Summary Table

Test	Role	What It Measures	Key Threshold	When to Use
OAE (TEOAE or DPOAE)	Screening (initial)	Outer hair cell function	Refer if >30-35 dB HL	All newborns; well-baby nursery screening
AABR	Screening (initial or second stage)	Cochlea-to-brainstem neural pathway	Refer if >40-45 dB HL	All NICU babies (mandatory); second stage for well-baby OAE refer
Diagnostic BERA (tone burst)	Gold standard for threshold estimation in infants	Frequency-specific air and bone conduction thresholds	Determines degree, type, and configuration per ear	All infants who fail screening; must be completed by age 2-3 months
ASSR	Supplementary / threshold estimation in severe-profound loss	Frequency-specific thresholds at high intensities	Used when BERA shows no response	ABD fitting decisions; profound loss evaluation
OAE (diagnostic)	Differential diagnosis	Outer hair cell integrity	Present = cochlear function intact; absent = cochlear or middle ear pathology	Differentiating ANSD from SNHL
Tympanometry	Middle ear assessment	Middle ear compliance and pressure	High-frequency (1000 Hz) probe for age <6 months; 226 Hz probe for age >6 months	Every diagnostic workup; confirm or exclude conductive component
Acoustic reflex	Supplementary	Brainstem auditory pathway integrity	Negative reflex predicts threshold >70 dB; absent in ANSD	Aid in ANSD diagnosis and threshold estimation
Behavioral audiometry	Cross-check principle	True perceptual hearing thresholds	BOA (0-6 months), VRA (5-36 months), Play audiometry (>24 months)	Must be done as soon as developmental age allows
MRI temporal bone/brain	Imaging (first line)	Inner ear anatomy, cochlear nerve, retrocochlear pathology	Cochlear nerve aplasia/hypoplasia, cochlear malformation	All confirmed SNHL cases; CI planning
HRCT temporal bone	Imaging (complementary)	Bony anatomy of inner/middle ear	Bony cochlear anatomy, ossicular chain, vestibular aqueduct	CI surgery planning; suspected ossification or facial nerve anomaly
Connexin-26 (GJB2) genetic test	Etiologic evaluation	Most common genetic mutation in nonsyndromic SNHL	Homozygous or compound heterozygous mutations	All confirmed SNHL; offer with genetic counseling
CMV PCR (urine/saliva)	Etiologic evaluation	Congenital CMV infection	Must be obtained within 3 weeks of life for congenital diagnosis	All confirmed SNHL; especially if progressive/unilateral
ECG	Syndromic screen	Cardiac conduction	Prolonged QTc suggests Jervell and Lange-Nielsen syndrome	All confirmed profound bilateral SNHL

The diagnostic approach follows a tiered logic, starting with screening and escalating to confirmatory testing.

Step 1: Newborn hearing screening. The best initial test for all newborns is either OAE or AABR, performed before hospital discharge and no later than age 1 month. OAE is fast and cheap, detecting outer hair cell dysfunction at a threshold of roughly 30-35 dB HL. AABR evaluates the entire peripheral auditory pathway up to the brainstem but has a slightly higher detection threshold (40-45 dB HL), meaning it may miss mild cochlear loss. The critical point: OAE alone will miss ANSD because outer hair cells are intact in that condition. For this reason, the guideline mandates AABR as the sole or combined screening modality for all NICU infants, given the higher prevalence of ANSD in that population.

Many programs use a two-stage protocol for well-baby nursery infants: OAE first, and if the baby refers, AABR is performed before discharge. A baby that fails OAE but passes AABR is considered to have passed the screen.

Step 2: Diagnostic confirmation. All infants who refer on screening must complete a comprehensive audiologic evaluation by age 2-3 months. The gold standard is diagnostic BERA with tone burst stimuli, which provides frequency-specific air- and bone-conduction threshold estimates per ear. Click-evoked BERA alone is insufficient because click is a broadband stimulus that cannot resolve hearing loss at individual frequencies, particularly sloping configurations.

When BERA shows no response at maximum output, high-intensity click testing with alternating polarity must be performed to evaluate for the presence of cochlear microphonic, the hallmark finding of ANSD.

ASSR is added when hearing loss is severe to profound, or when BERA provides no waveforms, because ASSR can estimate thresholds at higher stimulus intensities.

Step 3: Middle ear evaluation. Tympanometry is performed in every diagnostic workup to distinguish sensorineural from conductive or mixed hearing loss. For infants under 6 months of age, high-frequency tympanometry (1000 Hz probe tone) is required because the neonatal ear canal tends to collapse and the tympanic membrane resonates at higher frequencies due to its greater mass density. The standard 226 Hz probe tone may produce falsely normal results in this age group. Acoustic reflexes supplement the evaluation: an absent reflex predicts thresholds above 70 dB and is also a characteristic finding in ANSD.

Step 4: Behavioral cross-check. Electrophysiologic thresholds must be confirmed by behavioral testing as soon as the child's developmental age allows: BOA from 0-6 months (observational, not diagnostic), VRA from 6 months (conditioned response, yields reliable thresholds), and conditioned play audiometry from 24 months.

Step 5: Etiologic workup. All confirmed cases should be offered Connexin-26 genetic testing, urine/saliva CMV PCR (ideally within the first 3 weeks of life), and ECG to rule out long QT syndrome. MRI of the temporal bone is the first-line imaging study to visualize the cochlear nerve, membranous labyrinth, and brain parenchyma. HRCT is complementary when bony anatomy must be evaluated for cochlear implant surgery planning.

4. Management & Treatment

Summary Table

Stage	Intervention	Indication	Timing
EHDI 1-3-6 Principle	Screen, diagnose, intervene	All newborns	Screen by 1 month, diagnose by 3 months, intervene by 6 months
Hearing Aid (ABD)	Behind-the-ear (BTE) model; bilateral fitting	All degrees of SNHL (mild through profound) that interfere with development	Fitted by 4 months of age or as soon as diagnosis is confirmed
ABD trial for CI candidates	BTE with MPO/gain >130/75 dB SPL	Threshold 90-110 dB; mandatory for ANSD	Minimum 8 hr/day wear; evaluate at 3 and 6 months post-fitting
Cochlear Implant (CI)	Surgical implantation of electrode array into cochlea	Bilateral severe-to-profound SNHL (>70 dB), inadequate benefit from ABD	Ideally before 12 months; pre-lingual candidates best before 48 months; not recommended after age 7 without prior habilitation
Bilateral CI	Simultaneous or sequential	All bilateral CI candidates	Sequential: second implant within 1 year (max 5 years)
Speech-Language Habilitation	Auditory Verbal Therapy (AVT) is the primary method for children receiving ABD or CI	All children with confirmed hearing loss	Begins immediately after ABD fitting or CI switch-on
Sign Language	Indicated when auditory-oral approach is contraindicated or insufficient, or by family preference	Children with absent cochlear nerve, failed CI/ABD, or family choice	Concurrent with or as alternative to oral habilitation
Developmental Surveillance	KPSP questionnaire, Denver II, CAT-CLAMS, modified hearing function questionnaire (TDDM/LittlEARS)	All children regardless of screening result	Starting at age 2 months at primary care visits

Acute phase (0-6 months): The first priority after a confirmed diagnosis is ABD fitting, ideally by 4 months of age. The recommended type for children is the behind-the-ear (BTE) model because the ear continues to grow until puberty, and only the earmold (inexpensive) needs periodic replacement. Bilateral amplification is recommended for bilateral hearing loss regardless of symmetry. Fitting is verified using RECD (real ear to coupler difference) measurements or REAR (real-ear aided response). For ANSD, fitting is based on behavioral thresholds rather than BERA thresholds, and amplification is started at low gain and gradually increased.

Evaluation of ABD benefit (3-6 months post-fitting): The child should demonstrate aided thresholds of at least 40 dB across all frequencies and show measurable progress in auditory and language development assessed by the St. Gabriel Questionnaire at 3-month intervals. If two consecutive 3-month evaluations show no meaningful progress, the child should be referred for cochlear implant candidacy evaluation.

Cochlear implant candidacy: Criteria include (1) bilateral SNHL with threshold >70 dB on electrophysiologic testing confirmed by behavioral assessment, (2) failure of ABD trial as described above, (3) no medical or radiologic contraindications, (4) demonstrated family commitment to long-term habilitation, and (5) psychological/behavioral evaluation. For thresholds above 110 dB, the child may proceed directly to CI without an ABD trial. Implantation should occur as early as possible, with literature supporting surgery before 12 months of age for optimal language outcomes comparable to normal-hearing peers. The maximum recommended age for CI in a pre-lingual child without prior optimal habilitation is 7 years.

Bilateral CI is superior to unilateral for speech perception and sound localization. Simultaneous bilateral implantation is preferred. If sequential, the second implant should be placed within 1 year and no later than 5 years after the first.

Speech-language habilitation must begin immediately after device fitting or CI switch-on. The primary method recommended for children pursuing auditory-oral communication is Auditory Verbal Therapy (AVT), delivered by a certified AVT practitioner. AVT focuses on developing listening skills through the hearing device and building spoken language through a parent-centered coaching model. Other methods include sign language, total communication, and preverbal communication skills training. The choice of communication modality is made collaboratively with the family.

Contraindications and special considerations: Conductive hearing loss should be medically or surgically treated before ABD fitting. Children with cochlear nerve aplasia on MRI are not CI candidates and should be evaluated for Auditory Brainstem Implant (ABI). For ANSD, some children show spontaneous improvement by 18 months, so CI timing may be deferred with close monitoring of language development. Vaccination (particularly pneumococcal vaccine) is recommended prior to CI surgery to reduce the risk of post-implant meningitis.

5. Newborn Hearing Screening Program

EHDI 1-3-6 Framework

Milestone	Target Age	Action
Screen	Before discharge, no later than 1 month	OAE and/or AABR (electrophysiologic, objective testing)
Diagnose	No later than 3 months (newer EHDI 1-2-3 targets age 2 months)	Comprehensive audiologic evaluation (diagnostic BERA tone burst, OAE, tympanometry, acoustic reflexes)
Intervene	No later than 6 months (newer EHDI 1-2-3 targets age 3 months)	ABD fitting, CI referral if indicated, speech-language habilitation, family counseling

Screening Protocol by Population

Population	Screening Test	Protocol
Well-baby nursery	OAE or AABR (either technology acceptable)	Two-stage protocol preferred: if OAE refers, follow with AABR before discharge. Pass on either technology at both ears = pass. Refer on AABR = direct to outpatient rescreen.
NICU infant (>5 days stay)	AABR mandatory (OAE may be added)	AABR is required because of higher prevalence of ANSD in this population. If AABR refers, direct referral to ENT for rescreen and comprehensive audiologic evaluation including diagnostic ABR.
Born outside hospital / no screening facility	Kuesioner TDDM (modified hearing function test) or LittlEARS questionnaire	Preliminary subjective screen; must be followed by objective testing (OAE/AABR) at the nearest equipped facility before age 1 month.

Screening Flowchart

Step	Action	If PASS	If REFER
1. Birth to discharge	OAE or AABR (well-baby) / AABR (NICU)	Counsel parents on speech milestones; schedule surveillance at 2-month well-child visit	Proceed to in-hospital rescreen (Step 2)
2. In-hospital rescreen	Repeat with same or other technology. For initial AABR refer, rescreen with AABR only.	Discharge with surveillance plan	Refer to outpatient rescreen (Step 3)
3. Outpatient rescreen	Before age 1 month: OAE and/or AABR	Pass = surveillance plan	Refer to comprehensive audiologic evaluation (Step 4)
4. Diagnostic evaluation	By age 2-3 months: Diagnostic BERA (tone burst), OAE, high-frequency tympanometry, acoustic reflexes, behavioral observation	Normal hearing confirmed = continue developmental surveillance	Hearing loss confirmed = proceed to Step 5
5. Etiologic workup	GJB2 genetic testing, CMV PCR (urine/saliva), ECG, MRI temporal bone	Directed by results	Directed by results
6. Intervention	By age 6 months: ABD fitting, CI candidacy evaluation if indicated, speech-language habilitation referral, genetic counseling, family support	Ongoing monitoring	Ongoing monitoring
7. Ongoing surveillance	All children regardless of screening outcome: developmental monitoring using KPSP, modified hearing function questionnaire, Denver II at well-child visits starting at age 2 months	Continue through childhood	Refer for audiologic re-evaluation if any concern arises

Post-Screening Surveillance (Even If Pass)

The guideline emphasizes that all children, regardless of screening outcome and regardless of risk factor status, must receive ongoing communication development surveillance starting at age 2 months. This is because:

(a) Screening can miss mild hearing loss (below OAE/AABR thresholds), (b) progressive or late-onset hearing loss (e.g., CMV, enlarged vestibular aqueduct) may not be present at birth, and (c) ANSD may show transient improvement and later regression. Any child showing delayed speech/language milestones or whose parents express concern about hearing must be referred for full audiologic evaluation regardless of a prior pass result.

6. Differential Diagnosis & Distractors

Differential	Why It Looks Similar	Key Discriminator
Conductive hearing loss (otitis media with effusion, ossicular fixation)	Also presents with failed hearing screen, speech delay, and apparent inattention to sounds	Tympanometry is abnormal (flat type B); BERA shows air-bone gap; OAE may refer but cochlear function is intact. Resolves with medical/surgical treatment of middle ear disease.
Auditory Processing Disorder (APD)	Speech-language delay, difficulty understanding speech in noise, "hears but doesn't understand"	Normal audiometric thresholds on pure tone audiometry; normal OAE and ABR. APD is diagnosed in school-age children, not neonates.
Autism Spectrum Disorder (ASD)	Appears not to respond to name or voice, delayed language, social communication deficits. 30-40% of hearing-impaired children have comorbid neurobehavioral disorders	Normal audiogram in ASD (unless comorbid hearing loss). ASD has impaired social reciprocity, restricted interests, and repetitive behaviors. Always perform hearing evaluation as part of ASD workup.
Intellectual disability	Global developmental delay including language	Hearing evaluation is normal (or comorbid hearing loss must be excluded). Language delay is proportional to overall cognitive delay, not isolated.
Expressive language delay (isolated)	Delayed speech milestones with apparently normal hearing	Normal OAE, AABR, and behavioral audiometry. Receptive language is intact. No hearing threshold abnormality.
Auditory Neuropathy (ANSD) vs. cochlear SNHL	Both present with failed AABR and speech delay	In ANSD: OAE is present (intact outer hair cells); BERA shows cochlear microphonic that follows stimulus polarity reversal. In cochlear SNHL: OAE is absent. This distinction determines ABD fitting approach and CI timing.
Congenital CMV vs. genetic SNHL	Both present as bilateral SNHL in a newborn	CMV: may be progressive/fluctuating, may be unilateral or asymmetric, associated with periventricular calcifications, hepatosplenomegaly, petechiae, microcephaly. Diagnosed by urine/saliva CMV PCR within first 3 weeks of life. Genetic SNHL (Connexin-26): typically stable, bilateral, symmetric, no systemic findings.
Jervell and Lange-Nielsen syndrome vs. nonsyndromic profound SNHL	Both present as bilateral profound SNHL from birth	Jervell and Lange-Nielsen has prolonged QTc on ECG and risk of fatal cardiac arrhythmia (syncope, sudden death). This is why ECG is part of the standard workup for all profound bilateral SNHL.

7. Traps & High-Yield Pearls

The most common way students get questions on congenital SNHL wrong is by confusing the capabilities and limitations of OAE versus AABR. A vignette describing a NICU infant with hyperbilirubinemia requiring exchange transfusion who "passes OAE" but has delayed speech is testing your knowledge of ANSD. The student who sees "passed OAE" and concludes that hearing is normal will miss the diagnosis entirely. The correct reasoning is that OAE only tests outer hair cell function and does not evaluate neural transmission; AABR is required for NICU babies precisely because ANSD is prevalent in this population.

Another frequent trap involves the timeline. Test-writers will present a child diagnosed at 9 months of age with bilateral profound SNHL and ask for the next best step. The distractor answer is "start ABD." The correct answer for thresholds above 110 dB is direct CI referral without an obligatory ABD trial, because the guideline allows bypassing the trial at that severity. Conversely, for thresholds between 90 and 110 dB, an ABD trial is mandatory, and the student who jumps to CI referral without a documented ABD trial is wrong.

A third trap is the ECG question. A vignette describing a child with bilateral profound SNHL who suddenly collapses during exercise is testing whether you recognize Jervell and Lange-Nielsen syndrome (autosomal recessive SNHL + prolonged QT interval). The student who attributes the syncope to an unrelated cardiac condition without connecting it to the hearing loss will miss the underlying syndrome.

Finally, students must recognize that passing a newborn hearing screen does not rule out hearing loss permanently. Progressive or late-onset causes (CMV, enlarged vestibular aqueduct, certain genetic mutations) can develop after a normal screen. The core competency tested here is understanding that ongoing developmental surveillance with communication milestone monitoring is mandatory for every child, regardless of screening result, and any parental concern about hearing or language at any age warrants a full audiologic re-evaluation.

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