Page 1210 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1210

Eyes                                          1185



  VetBooks.ir  surface due to thickening of the epithelial layer, and   out other causes of keratitis, including viral infection
                                                         (EHV-2 and -5), mycoses, corneal abscess, eosino-
          sometimes, cellular infiltrate into the superficial
          stroma (Fig. 11.96). Superficially branching corneal
          neovascularisation  with corneal oedema is  usually   philic keratoconjunctivitis, KCS, foreign bodies,
                                                         physical irritation associated with distichiasis, ecto-
          present.                                       pic cilia and entropion, neurotrophic keratitis, and
                                                         exposure keratopathy due to facial nerve dysfunction
          Deep/mid-stromal IMMK                          or lagophthalmos associated with exophthalmia or
          This form of IMMK is associated with extensive   buphthalmia.
          mid- to deep stromal vascularisation, oedema, cel-
          lular infiltration and scarring (Fig. 11.97). Despite  Diagnosis
          the extensive pathology these patients may be rela-  Diagnosis  is based on identifying  the character-
          tively comfortable. The disease may cycle through   istic corneal pathology associated with the three
          relatively quiescent periods followed by recurrence   subtypes of IMMK and ruling out other potential
          of active disease episodes.                    causes of corneal pathology. A subsequent response
                                                         to anti-inflammatory treatment helps strengthen the
          Endotheliitis                                  diagnosis of IMMK.
          In this form of IMMK the corneal endothelium
          is affected, leading to varying degrees of corneal  Management
          oedema subsequent to disruption of the endothelial   Early diagnosis and initiation of treatment is impor-
          pump mechanism. The oedema may vary from mild   tant  to  minimise  the  recruitment of  inflamma-
          to severe, with corneal decompensation (corneal   tory cells to the cornea, which causes IMMK to
          hydrops) occurring in some patients. Deep corneal   become increasingly refractive to medical manage-
          vascularisation and cellular infiltration including   ment with time. Medical treatment includes topi-
          clumps of cells on the endothelium may be present   cal corticosteroids (1% prednisolone acetate, 0.1%
          (Figs. 11.98, 11.99). Concurrent anterior uveitis   dexamethasone), NSAIDs (flunixin meglumine,
          and pain may be present in some patients.      phenylbutazone) and immunosuppressive therapy
                                                         (cyclosporine A [CsA] and tacrolimus). The response
          Differential diagnosis                         to  anti-inflammatory  treatment  is  not  predictable
          There is no specific test for definitive diagnosis of   and various combinations of anti-inflammatory and
          IMMK, and therefore the diagnosis relies on ruling   immunosuppressive therapy may need to be trialled.




          11.96                                          11.97
















          Fig. 11.96  Superficial IMMK in a Thoroughbred   Fig. 11.97  Mid-stromal IMMK in a Warmblood
          gelding. Multifocal corneal epithelial and superficial   mare. There is extensive deep corneal stromal
          stromal opacities are affecting a geographical region   vascularisation, a haze to the central ventral cornea
          of the ventral cornea.                         with dense multifocal yellowish infiltrates and some
                                                         superficial pigment deposition.
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