Felis ISSN 2398-2950

Deafness: acquired

Contributor(s): Agnes Delauche, Rosanna Marsella

Introduction

  • Rare.
  • Non-hereditary deafness.
  • Two forms: conductive abnormalities due to outer and/or middle ear pathology; sensorineural due to cochlear abnormalities.
  • Cause: infection, ototoxins, presbycusis (deterioration due to ageing), trauma, fetal damage (intrauterine infection or drug toxicity) or malformation.
  • Signs: often missed. Partial, unilateral or bilateral hearing loss.
  • Diagnosis: signs.
  • Treatment: none.
  • Prognosis: guarded.
    Print off the owner factsheet Living with a deaf cat Living with a deaf cat to give to your client.

Pathogenesis

Etiology

Infections

Ototoxicity

  • Drugs or chemicals that damage either the sensory hair cells in the cochlea, or the stria vascularis.
  • Include: aminoglycosides, diuretics, eg furosemide Furosemide, antineoplastic drugs, eg vincristine Vincristine, other antibiotics, eg erythromycin Erythromycin, topical antiseptics, eg cetrimide and various other agents, eg ceruminolytics, prednisolone Prednisolone, salicylates  Acetyl salicylic acid, detergents.
    Ototoxicity of compounds varies greatly. Effect may be compounded by simultaneous use of two drugs at correct dosage eg loop diuretics and aminoglycosides.

Presbycusis

  • Ageing.

Trauma

  • Physical or acoustic (selective frequency deafness).

Fetal

  • Intrauterine infection, toxicity, anoxia.

Pathophysiology

  • Occlusion of external ear canal.
  • Destruction of tympanic membrane and structures of middle ear.
  • Damage to anatomy of inner ear.
  • Sensorineural deficits.
  • Otitis externa   →   stenotic external canal occluded with cerumen   →   conductive deafness.
  • Otitis media/interna   →   destruction of tympanic membrane and middle ear structures   →   conductive deafness.
  • Hemotogenous or exogenous infection   →   labyrinthitis (inflammation of inner ear)   →   sensorineural deafness. Associated vestibular deficits Vestibular disease.
  • Systemic aminoglycoside toxicity   →   theory: drug binds to glycosaminoglycans in stria vascularis of cochlear canal   →   disrupts phosphoinositide metabolism   →   sequential and progressive destruction of cochlear hair cells.
  • Topical application toxicity with ruptured tympanum   →   drug reaches inner ear   →   absorbed into cochlea.
    It has been suggested that topical applications according to recommended dosage even where the tympanum is ruptured can be assumed to be safe, although this is not guaranteed.
    Ototoxicity of drugs may be increased by anesthesia, previous cochlear damage, age and infection. Successive courses of treatment may have a cumulative effect.
  • Presbycusis   →   progressive pathology of middle ear structures   →   impaired articulation between tympanum and ossicles.
  • Acoustic trauma   →   increased shearing force   →   breaks cochlear hairs. May damage tympanic membrane and ossicles.

Diagnosis

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Gregory S P (2000) Middle ear disease associated with congenital palative defects in seven dogs and one cat. JSAP 41 (9), 398-401 PubMed.
  • Strain G M (1996) Aetiology, prevalence and diagnosis of deafness in dogs and cats. BVJ 152 (1), 17-36 VetMedResource.
  • Strain G M (1991) Congenital deafness in dogs and cats. Compend Contin Educ 13 (2), 245-50 VetMedResource.


ADDED