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Section 5 — General NICU Care / Supportive Care Pending expert review v1.0 · July 2026

Chapter 5.8 — Neonatal Sensory Screening & the EENT/Airway Examination (Eye, Ear, Airway)

Board-review synthesis · pending expert review

Educational guideline — verify locally. Complements ROP (02-07), neonatal airway anomalies (06-08), and ophthalmia neonatorum (08-08). Cross-references: CMV (infectious), kernicterus (10-01), CHARGE/22q11.2 (genetic).

1. Clinical Overview

Clinical Overview

The special senses and the airway share a feature: each is a structure whose failure is invisible until catastrophic, so each is approached by examination and screening rather than by waiting for symptoms. A newborn cannot report that it cannot see or hear, and an infant with a marginal airway may look well until it feeds, sleeps, or becomes ill. The recurring imperative is to look, screen, and anticipate — because the window in which intervention preserves function is narrow and closes quietly.

2. Key Clinical Points

Key Clinical Points
  • The red reflex asks one question — is the visual axis clear? A normal reflex is present, bright, and symmetric; any absent/dim/white(leukocoria)/asymmetric reflex is an URGENT referral.
  • Leukocoria is retinoblastoma (commonest childhood intraocular malignancy; sight- and life-threatening, may be hereditary/bilateral) until proven otherwise; also cataract, severe ROP, retinal detachment. Congenital cataract → deprivation amblyopia if not removed early (investigate galactosaemia, congenital infection). Because the visual cortex needs a clear image, visual-axis obstruction in infancy is urgent, never elective.
  • Congenital glaucoma triad: tearing, photophobia, blepharospasm with an enlarged cloudy cornea — an emergency. Constant strabismus (or any persisting beyond a few months) and neonatal nystagmus warrant referral.
  • ROP is a two-phase disease: relative hyperoxia arrests peripheral vessel growth (phase 1) → avascular hypoxic retina drives destructive neovascularisation (phase 2). Oxygen is targeted (not maximised); fluctuation and poor postnatal growth add risk. Described by zone (posterior/smaller = worse), stage, and plus disease (active — key treatment indicator). Asymptomatic → detected by scheduled screening; most regresses (screen and observe) while plus/aggressive-posterior disease prompts treatment (laser/anti-VEGF). Cerebral visual impairment (normal eye, injured pathways) is common and easily missed.
  • Universal newborn hearing screening uses OAE (test up to the cochlea — MISS auditory neuropathy) and ABR (detect auditory neuropathy). NICU graduates (at risk of auditory neuropathy via prematurity and hyperbilirubinaemia) are screened with ABR. Early identification, amplification, and cochlear implantation within the language window allow near-normal language; delay cannot be recovered.
  • A passed screen does not end surveillance: congenital CMV (leading non-genetic cause) causes late-onset/progressive loss; any child with language delay needs formal hearing testing regardless of a passed screen. Genetic causes are common (connexin/GJB2 non-syndromic; syndromes — Waardenburg, Usher, Pendred, Alport, Jervell-Lange-Nielsen [long QT]).
  • The external/middle ear shares a branchial origin with the face/jaw (external anomalies accompany craniofacial anomalies and conductive loss); the inner ear develops separately (a normal pinna does not exclude sensorineural deafness).
  • Choanal atresia (obligate nasal breather): bilateral → cyanotic at rest, pink with crying; bedside test = catheter cannot pass through the nose; establish an oral airway, definitive treatment surgical; associated with CHARGE. Micrognathia (Pierre Robin sequence: micrognathia → glossoptosis → pharyngeal obstruction + cleft palate; Stickler syndrome) obstruction is relieved by PRONE positioning ± nasopharyngeal airway. Isolated cleft palate → palpate/inspect every palate; associated with Robin sequence and 22q11.2 deletion.
  • Anticipate the difficult airway from the face and history (micrognathia, midface hypoplasia, large tongue, limited mouth opening); plan delivery/airway management with senior/specialist personnel and difficult-airway equipment before the emergency.
  • Stridor timing localises obstruction: inspiratory = extrathoracic; expiratory = intrathoracic; biphasic = fixed (subglottic/external). Laryngomalacia is the commonest cause (inspiratory, worse supine/feeding/crying, better prone; worsens over months then resolves) — red flags (feeding difficulty, aspiration, failure to thrive, hypoxaemia) mean significant disease. Acquired subglottic stenosis from prolonged/traumatic intubation presents as repeated failed extubation or post-extubation stridor — prevention (right-sized tube with a leak, minimal duration/attempts) is the point.
  • Bilateral vocal cord paralysis → significant stridor with a relatively normal cry (look for Chiari/hydrocephalus); subglottic haemangioma → biphasic stridor at a few months, suspect with beard-distribution cutaneous haemangiomas (propranolol); vascular ring → biphasic stridor with feeding difficulty.

3. References to Verify

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