Posterior segment diseases

Abstract

Summary Diseases of the vitreous, fundus and optic nerve are described and illustrated according to their ophthalmological appearance. Vitreal alterations are commonly of developmental, degenerative, age related, traumatic or inflammatory origin and of minor clinical relevance. In contrast, those affecting the fundus, may be accompanied by visual deficits or blindness. Fundic lesions of inflammatory (multifocal or peripapillary chorioretinitis, haemorrhage, retinal detachment) and traumatic origin have to be differentiated from congenital (congenital stationary night blindness, colobomatous defects, retinal dysplasia), degenerative (cystic retinal degeneration), metabolic (equine motor neuron disease), neoplastic and age related alterations (senile retinopathy). Inflammation (acute neurochorioretinitis) and ischaemia (ischaemic neuro‐chorioretinopathy) involving the optic nerve will lead to blindness. The optic disc can be aplastic/hypoplastic or excavated due to coloboma or glaucoma, affected by ligation of the carotid and palatine arteries. Optic disc masses may arise due to inflammation, severe systemic haemorrhage, neoplasia or trauma. Lesions of the retrobulbar optic nerve can be caused by Borna virus infection, fungal granuloma, toxic insult, halicephalobiasis, trauma, severe blood loss and infection of the sphenopalatine sinus.

Eye examination as part of the equine prepurchase examination

“…() It is important that the clinician is familiar with these variants, and is confident with their recognition. One normal variant commonly confused with retinal ‘haemorrhage’ is the presence of the vascular reflex of the four large vortex veins, draining the posterior uvea, observed tracking across the tapetal fundus to exit the globe at the dorsal scleral foramen located dorsolaterally to the optic disc ( Fig ) (Matthews ; Nell and Walde ).…”

Electroretinogram evaluation of equine eyes with extensive ‘bullet‐hole’ fundic lesions

“…noted hyperfluorescence to focal depigmented lesions in the nontapetal fundus which occurred in three ponies 6 to 8 weeks following experimental intranasal EHV‐1 infection and speculated choroidal infarction as a cause, but did not note retinal vascular phase deficits or leakage to suggest peripapillary retinal compromise . A more recent publication points out that infarction of the choroidal vasculature would be expected to appear as nonfluorescing, dark areas on fluorescein angiography which is inconsistent with the previous description …”

“…As is consistent with a claim in the literature and personal experience, no evidence of active chorioretinal disease or bullet‐hole lesion progression was noted in either of these patients. Nell and Walde do state that widespread occurrence of bullet‐hole lesions may lead to progressive fundus degeneration accompanied by subtle to obvious visual impairment, but that did not occur in these two horses with extensive lesions. Both horses were reexamined 16 months following ERG assessment for a total of 34–40 months follow‐up with no changes noted.…”

“…Studies in foals and ponies experimentally infected with EHV‐1 demonstrated development of similar‐appearing lesions, which supports viral infection as an etiology . An association with equine leptospirosis or a different causative agent of equine recurrent uveitis has also been discussed, and bullet‐hole chorioretinal lesions may occur in association with peripapillary chorioretinitis or ‘butterfly’ lesions …”

Synopsis of Equine Veterinary Journal Supplement 37: Equine Ophthalmology III ‘Reviews in memory of Keith Barnett’. Part 2

“…This is the focus of the next paper, in which Professor Nell of the University of Vienna and a former colleague from the same institution, Professor Walde, provide a very comprehensive review of posterior segment disease (i.e. vitreous, retina and optic nerve) [11]. Many of the pathologies described need to be ‘seen’ to be understood, and to this end the paper is superbly illustrated.…”