Canis ISSN: 2398-2942

Deafness: acquired

Contributor(s): Kyle Braund, Agnes Delauche

Introduction

  • Rare but probably under-diagnosed.
  • 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 (intra-uterine infection or drug toxicity) or malformation.
  • Signs: often missed. Partial, unilateral or bilateral hearing loss.
  • Diagnosis: signs, brain stem auditory evoked potentials.
  • Treatment: usually no treatment by time diagnosed.
  • Prognosis: no cure but unilaterally deaf animals can lead a normal life.
    Print off the owner factsheet on Living with a deaf dog Living with a deaf dog 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 frusemide Furosemide ; antineoplastic drugs, eg vincristine Vincristine ; other antibiotics, eg erythromycin Erythromycin ; topical antiseptics, eg cetrimide; various other agents, eg ceruminolytics, prednisolone, salicylates, 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, eg shooting may affect gundogs).
Fetal
  • Intra-uterine 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 defecits.
  • Otitis externa Skin: otitis externa → stenotic external canal occluded with cerumen → conductive deafness.
  • Otitis media Otitis media /interna Otitis 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.
  • 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.
  • Accoustic trauma → increased shearing force → breaks cochlear hairs. May damage tympanic membrane and ossicles.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Gregory S P (2000) Middle ear disease associated with congenital palatine defects in seven dogs and one cat. JSAP 41 (9), 398-401 PubMed.
  • Shimada A et al (1998) Age-related changes in the cochlea and cochlear nuclei of dogs. J Vet Med Sci 60 (1), 41-48 PubMed.
  • Strain G M (1996) Aetiology, prevalence and diagnosis of deafness in dogs and cats. Br Vet J 152 (1), 17-36 PubMed.

Other sources of information

  • Knowles K (2000)Deafness in dogs and cats.In:Current Veterinary Therapy XII.Ed: R W Kirk. Philadelphia: W B Saunders. pp 971-974.


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