Conductive Hearing Loss

Aetiology / Classification

1. Obstruction of the external auditory canal
2. Tympanic membrane problems
3. Middle ear problems
4. Congenital abnormalities

1. Obstruction

Normal external auditory canal:

• Average diameter ~6 mm; average length ~25 mm
• Resonance frequency ≈ 3500 Hz
• Reverberatory contribution ≈ 10 dB near resonance
• Complete obstruction → CHL up to ~30 dB

Mechanisms for CHL due to obstruction:

• Immobility of TM from obstructing process
• Direct occlusion of the canal

Causes:

• Infectious: acute/chronic otitis externa (bacterial, viral, fungal) and media → inflammatory occlusion; furunculosis; chondritis; perichondritis; relapsing polychondritis; cellulitis
• Trauma: laceration ± clot, burns, cauliflower ear, avulsion, penetrating wounds, instrumentation/cleaning
• Inflammatory: e.g., Wegener’s granulomatosis
• Foreign bodies and cerumen impaction
• Neoplastic (rare): benign and malignant
• Benign:
  • Keratosis obturans / EAM cholesteatoma (EAMC): desquamated keratin accumulation
  • Exostoses: most common solid tumors of EAC; multiple, bilateral; smooth rounded nodules; associated with cold-water swimming
  • Osteomas: less common, pedunculated, usually single, along suture lines
  • Adenoma and ceruminoma
• Malignant: primary (SCC, BCC), secondary (e.g., melanoma), sebaceous carcinoma
• Degenerative: osteopetrosis, Paget’s disease, osteogenesis imperfecta

2. Tympanic Membrane (TM) Problems

a. Perforation

Mechanisms → CHL:

• Loss of effective airborne sound-receiving surface area
• Sound distortion at torn edge
• Baffle effect
• Rebound effect
• Degree of HL depends on size, location, and characteristics; tends to affect low frequencies

b. Others

Additional TM pathologies may contribute to CHL (as clinically relevant).

3. Middle Ear Problems

• i. Effusion: serous, purulent, sanguineous, barotrauma-related
• ii. Neoplasms: benign (e.g., cholesteatoma, adenoma); malignant (e.g., adenoid cystic carcinoma)
• iii. Ossicular chain problems

a. Ossicular fixation

• CHL due to increased resistance across compliance-dominated low and inertia-dominated high frequencies
• Causes: otosclerosis; tympanosclerosis with hyalinized connective tissue; postoperative or postinfectious scarring; passive restriction by adjacent structures
• Mass lesions (cholesteatoma, glomus tympanicum/jugulare, high jugular bulb) may impede stapes mobility

b. Ossicular discontinuity

• Infection/trauma risk devascularization of incudostapedial joint (suspended, vascular supply along incus long process and stapes suprastructure)
• Temporal bone fractures: longitudinal (more common), transverse
• If IS joint completely separated:
  • Maximal CHL with intact TM
  • With TM perforation, maximal CHL may not manifest (oval/round window phase difference preserved)
• Tympanogram/pneumatic otomicroscopy: abnormally high compliance and excessive excursion
• If soft tissue bridges maintain IS spacing: low frequencies transmitted; high frequencies lost

iv. Neoplasms

• Benign: neurofibroma, hemangioma, hemangiopericytoma, fibrous dysplasia
• Malignant: rhabdomyosarcoma, lymphangioma, leukemia, multiple myeloma, paraganglioma

v. Inflammatory

• Wegener’s granulomatosis, polyarteritis nodosa, eosinophilic granuloma (Hand–Christian–Schüller disease), sarcoidosis, mucopolysaccharidoses

vi. Iatrogenic

• Surgical failure, keloid

vii. Negative pressure

• Goode (1980): negative ME pressure (~100 mm H2O) reduces TM excursion → “the worse the negative pressure, the worse the hearing.”

4. Congenital Malformation

• Auricle, EAC, middle ear, and ossicles may develop independently (Anson & Donaldson, 1981)
• Maximal losses with bony atresias
• Causes/syndromes: Apert’s disease, Goldenhar’s syndrome, Turner’s syndrome, achondroplasia, Marfan’s syndrome, Treacher Collins, Mohr’s syndrome, Pierre Robin, microtia, otofacial cervical synd., otopalatal–digital synd., congenital–hereditary, anotia, cup ear deformity

Nature of Sound and Physiology of Conductive Sound Transfer

Wave character of sound transmission

Sound is mechanical vibration ~20 Hz to 20 kHz.

Acoustic impedance

• Air and perilymph have different acoustic impedances
• Interface between different impedances → partial reflection and transmission
• Direct air-to-perilymph coupling would reflect >99.9% of acoustic energy

Impedance-matching transformers and the middle ear

• Middle ear functions as an impedance-matching transformer
• Large TM area captures airborne sound; small oval window couples into perilymph
• Three components:
  • Area ratio: TM to oval window
  • Lever ratio: manubrium of malleus vs long process of incus
  • Shape-related contribution of TM
• Overall impedance transformation ≈ 185:1 (Pickles, 1982)

Tympanic membrane

• Oblique plane, near-continuation of posterior EAC wall
• Compliant due to catenary curvature → large excursions for low frequencies
• Effective area ≈ 65% of anatomic area (~85 mm² total)

Ossicular chain

• Moves primarily as rigid-body rotations (frequency-dependent inertial properties)
• Altering mass/inertia (disease/surgery) impacts transmission differently across frequencies
• Axis of rotation: along line from incus short process tip through anterior malleal ligament (Bàràny, 1938)
• “Biting” mechanism of incudomalleolar–incudostapedial complex prevents stapes avulsion with outward TM motion

Understanding small

• Loudest sound pressure disturbances ≈ 30 Pa vs atmospheric >100,000 Pa
• Just audible at 1 kHz ≈ 0.00003 Pa; displacements far below atomic spacings
• “Nudging” middle ear prostheses at surgery is orders of magnitude more motion than encountered in vivo during use

Bibliography

• Cummings, C. Otolaryngology. Chapter 175