ISSN 2398-2977      

Eye: glaucoma

pequis

Introduction

  • A group of disorders associated with impaired aqueous outflow and elevated intraocular pressure, resulting in irreversible optic nerve damage and ultimately vision loss.
  • Cause: most commonly secondary to uveitis but may be primary (unrelated to other ocular disease). Primary glaucoma may be congenital.
  • Signs:
    • Acute glaucoma: elevated intraocular pressure, variable degree of corneal edema, mydriasis.
    • Chronic glaucoma: buphthalmos (globe enlargement), corneal edema and striae (deep stromal opacities representing breaks in Descemet's membrane), mydriasis, possible lens luxation, optic nerve and retinal atrophy, vision loss.
  • Diagnosis: tonometry and clinical signs.
  • Treatment: involves medical enhancement of aqueous outflow, decrease in aqueous humor production, surgical ablation of ciliary body or enucleation/prosthesis for blind and intractably painful eyes.
  • Prognosis: long-term prognosis is poor - enucleation may be necessary.
Print off the Owner factsheet on Common eye problems to give to your clients.

Pathogenesis

Etiology

Congenital
  • Aplasia or dysgenesis of iridocorneal angle.

Primary

  • Abnormality in aqueous humor outflow of unknown mechanism.
  • Possible developmental abnormality of drainage angle.
  • Familial tendency may exist.

Secondary

Pathophysiology

  • Group of disorders associated with elevated intraocular pressure (IOP) resulting in permanent optic nerve damage and blindness.
  • All forms in the horse are caused by interference with aqueous humor outflow.
  • 3 categories recognized:
    • Primary (least common).
    • Secondary (most common).
    • Congenital.
  • Aqueous humor is produced by the ciliary body by energy-dependent/energy-independent mechanisms. The enzyme carbonic anhydrase is an important contributor.
  • The aqueous humor passes via the posterior chamber through the pupil into the anterior chamber and exits through the iridocorneal angle (conventional outflow pathway) or the uveovortex/uveoscleral pathway (unconventional outflow pathway).
  • The outflow systems are particularly extensive and low resistance in the horse   →   low incidence of glaucoma in the uveitis-damaged eye.
  • In secondary glaucoma several mechanisms individually or collectively can block the aqueous humor outflow:
    • Contraction of pre-iridial post-inflammatory fibrovascular membranes.
    • Inflammatory debris obstructing the ventral drainage angle.
    • Adherent miotic pupil   →   pupillary block and iris bombe   →   trabecular compression and angle closure.
    • Post-inflammatory uveal atrophy   →   angle collapse.
    • Anterior lens luxation and vitreal prolapse compressing the drainage angle.
    • Obstruction of angle by neoplastic cells.
  • IOP elevation   →   obstruction of optic nerve axoplasmic flow at the lamina cribrosa   →   progressive damage to the retinal ganglion cells and optic nerve areas   →   visual deterioration and blindness.

Timecourse

  • Acute cases may appear within 24 h of intraocular disease.
  • Chronic fluctuant cases over weeks/months are more common.

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.
  • Annear M J, Gemensky-Metzler A J & Wilkie D A (2012) Uveitic glaucoma in the horse. Equine Vet Educ 24 (2), 97-105 VetMedResource.
  • Ollivier F & Monclin S (2010) Equine glaucomas. Equine Vet Educ 22 (6), 299-305 VetMedResource.
  • Ollivier F J, Sanchez R F & Monclin S J (2009) Equine glaucomas: A review. Equine Vet Educ 21 (5), 232-235 VetMedResource.
  • Komáromy A M, Garg C D, Ying G S & Liu C (2006) Effect of head position on intraocular pressure in horses. Am J Vet Res 67 (7), 1232-1235 PubMed.
  • Willis A M, Diehl K A, Hoshaw-Woodard S et al (2001) Effects of topical administration of 0.005% latanoprost solution on eyes of clinically normal horses. Am J Vet Res 62, 1945-1951 PubMed.
  • Willis A M, Robbin T E, Hoshaw-Woodard S et al (2001) Effect of topical administration of 2% dorzlamide hydrochloride or 2% dorzlamide hydrochloride-0.5% timolol maleate on intraocular pressure in clinically normal horses. Am J Vet Res 62 (5), 709-713 PubMed.
  • Cullen C L & Grahn B H (2000) Equine glaucoma - a retrospective study of 13 cases presented at the Western College of Veterinary Medicine from 1992-1999. Can Vet J 41 (6), 470-480 PubMed.
  • Herring I P, Pickett J P, Champagne E S et al (2000) Effect of topical 1% atropine sulfate on intraocular pressure in normal horses. Vet Ophthal 3, 139-143 PubMed.
  • Whigham H M, Brooks D E, Andrew S E et al (1999) Treatment of equine glaucoma by transscleral neodymium:yttrium aluminum garnet laser cyclophotocoagulation - a retrospective study of 23 eyes of 16 horses. Vet Ophthal 2, 243-250 PubMed.
  • Miller T R et al (1995) Equine glaucoma: Clinical findings and response to treatment in 14 horses. Vet Comp Ophthal (3), 170-182 VetMedResource.
  • Wilcock B P, Brooks D E and Latimer C A (1991) Glaucoma in horses. Vet Patho 28, 74-78 PubMed.
  • Barnett K C et al (1988) Buphthalmos in a Thoroughbred foal. Equine Vet J 20, 132-135 PubMed.

Other sources of information

  • Lassaline M E & Brooks D E (2005) Equine Glaucoma. In: Equine Ophthalmology. Ed: Gilger B C. Elsevier Saunders.
  • Gliger B C (2003) How to Diagnose and Treat Glaucoma in the Horse. In: Proc 49th AAEP Convention. pp 306-311.
  • Brooks D E (1999) Equine Ophthamology. In: Veterinary Ophthamology. 3rd edn. Ed: Gelatt K N. Lippincott.

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