Page 1226 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1226

Eyes                                          1201



  VetBooks.ir  the fixed intracanalicular portion of the optic nerves.   11.110
          This may cause stretching, shearing and/or avulsion
          of the  retinal ganglion cell  axons/optic nerve(s) or
          chiasm, resulting in optic nerve atrophy and sudden
          blindness. Partial or complete visual loss occurs in
          the affected eye(s) within 24 hours of injury.

          Clinical presentation
          Horses with traumatic optic neuropathy present
          with a history of sudden onset of blindness with or
          without a known history of trauma. The pupil(s) is
          (are) fixed and dilated with sluggish to absent PLRs
          in  the affected  eye(s).  Ophthalmic lesions are  not
          usually seen initially because of the often retrobul-
          bar nature of the injury.
            Ophthalmoscopic lesions, including peripapillary
          and/or ONH oedema or haemorrhage and exudation
          into the vitreous may be present within 24–48 hours   Fig. 11.110  Traumatic optic neuropathy. This horse
          of injury (Fig. 11.110). With chronicity, the lamina   presented blind and was suspected to have fallen
          cribrosa becomes more prominent, the ONH will   backwards after rearing up. Note the peripapillary
          appear pale and atrophied, the peripapillary retinal   and ONH haemorrhages, as well as haemorrhagic
          vessels will appear diminished/attenuated, and focal   streaming into the vitreous.
          grey patches medial, lateral and ventral to the ONH,
          indicating choroidal degeneration, may also be seen
          (Fig. 11.111).                                 11.111


          Differential diagnosis
          Optic nerve and retinal degeneration in the horse
          has been reported to develop secondary to ERU,
          glaucoma, hypovolaemia/blood loss, exposure to
          toxins, progressive retinal atrophy and carotid artery
          ligation. Other differentials include exudative optic
          neuropathy and optic neuritis. Brain injuries should
          also be considered in the list of differential diagnoses
          for traumatic optic neuropathy.

          Diagnosis
          Diagnosis should be based on history and findings
          on physical and ophthalmic examination. A failure
          to navigate photopic and scotopic maze tests is also
          observed.
                                                         Fig. 11.111  Chronic traumatic optic neuropathy.
          Management                                     This yearling fell over backwards 2 months previously
          Treatment when cases are presented acutely tradi-  and was immediately blind but without any fundic
          tionally involves high doses of anti-inflammatories   changes. The fundus of both eyes now shows classic
          such as systemic corticosteroids (e.g. dexametha-  changes of the condition in the optic disc and tapetal/
          sone), NSAIDs and dimethylsulphoxide in order to   non-tapetal fundus. (Photo courtesy GA Munroe)
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