View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Digital Repository @ Iowa State University Volume 55 | Issue 1 Article 10 1993 Glaucoma: Past and Present Management Techniques David M. Tinsley Iowa State University Daniel M. Betts Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Eye Diseases Commons, Therapeutics Commons, and the Veterinary Medicine Commons Recommended Citation Tinsley, David M. and Betts, aD niel M. (1993) "Glaucoma: Past and Present Management Techniques," Iowa State University Veterinarian: Vol. 55 : Iss. 1 , Article 10. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol55/iss1/10 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. GLAUCOMA: PAST AND PRESENT MANAGEMENTTECHNIQUES David M. Tinsley, D.V.M.* Daniel M. Betts, D.V.M., MSc., Dip.ACVO.** Abstract away from the globe. This conventional "corneoscleral" route accounts for 85-900/0 of the This article reviews the clinical signs and total aqueous outflow.2 The remaining 10-15% diagnostic modalities appropriate for glaucoma. exits via the unconventional "uveoscleral" Classification of this disease and currently outflow diffusing posteriorly through the iris, recommended treatment options are discussed. ciliary body, and choroid into the suprachoroidal 2 space and adjacent sclera. In order to have an Introduction increased lOP, there must be either an in­ creased production or decreased outflow. Glaucoma is a group of eye diseases Increased production (hyperfiltration) has never characterized by an increase in intraocular been documented, hence, all glaucomas are pressure which causes pathological changes in based on impaired circulation or outflow. the optic disc and typical defects in the field of vision. 1 Generally accepted normal intraocular Diagnosis-Clinical Signs pressure (lOP) readings in the dog and cat range from 15-30 mmHg. Maintenance of Early recognition of glaucoma is mandatory if normal pressure is through a delicate balance of successful regulation of intraocular pressure aqueous production and outflow. The formation with subsequent preservation of vision is to be of aqueous 11umor is dependent on three achieved. Establishing a diagnosis of glaucoma dynamic processes. Active transport is the most is based exclusively on measurement of the important of the three and results in the move­ intraocular pressure. If such diagnostics are to ment of Na+ ions from the blood into the be performed, the clinician must first have a aqueous humor against a concentration gradient reasonable index of suspicion that the disease through the use of energy dependent Na+/K+ is in fact present. As a rule, the presenting ATPase pumps located in the non-pigmented history is unlikely to be of much value. With this epithelial cells overlying the ciliary body pro­ in mind, initial physical examination findings are 2 cesses. Carbonic anhydrase catalyzes the often the first reliable tool available to the - reaction: CO2 + H20 <-> H2C03 + HC03 <->H+. clinician in establishing the diagnosis. Unfortu­ Entry of bicarbonate is associated with influx of nately, those clinical signs that are consistently water into the posterior chamber. The remain­ expressed in acute glaucoma mimic those of the der is a cornbination of solute movement down a more commonly presented extraocular red eye concentration gradient (passive diffusion), as disorders. These include lacrimation, well as movement across cell mefl1branes photophobia, blepharospasm and variable secondary to local hydrostatic forces (ultrafiltra­ congestion of the conjunctival/episcleral vessels tion). Resultant aqueous humor collects in the secondary to shunting of aqueous/venous posterior chamber of the globe. It then flows outflow (Fig. 1). Where lOP exceeds 40 - 45 through the pupillary apel1ure, anterior chamber, mmHg, corneal stromal edema develops pectinate ligaments, trabecular meshwork of the secondary to impaired dehydration by the ciliary cleft, scleral venous plexus to be trans­ endothelial based Na+/K+ ATPase pump. ported via the local efferent vascular channels Mydriasis is an important clinical finding which can aid in differentiating glaucoma 'from uveitis. *Dr. Tinsley is a Resident in the Ophthalmology This loss of tone to the constrictor pupillae is a Clinical Scinences Dept. at Iowa State College sequelae to extinguished retinal stimulation and of Veterinary Medicine. direct pressure effects on the iris stroma (Fig. 2). **Dr. Betts is an Ophthalmology Professor in the Blindness results from retinal ischemia as Deparrtmint of Veterinary Clinical Sciences at elevated lOP prevents normal hemodynamic Iowa State University. flow to this tissue. Therapy instituted to 36 Iowa State University Veterinarian normalize lOP may reoxygenate retinal photore­ Table 2 ceptors in time to restore vision. Digital palpa­ Clinical Signs of Chronic Glaucoma tion of the globe may reveal a "hard eye". This 1. Continued engorgement of conjunctival technique is inconsistently reliable in cases of episcleral vasculature moderate pressure elevations. 2. Buphthalmos As the disease progresses, signs that were 3. Blindness initially variable (Table 1) become reliably 4. Corneal edema present. With chronicity, elevated lOP results in 5. Striate keratopathy enlargement of the globe (buphthalmos), 6. Equatorial staphyloma thinning of the equatorial sclera with uveal 7. Mydriasis herniation (equatorial staphyloma) and rupture 8. Lens luxation/subluxation of Descemet's membrane. Ensuing full thick­ 9. Cataracts ness corneal edema is seen clinically as linear 10. Liquefaction of the vitreous (syneresis) white fissure in the stroma (Fig. 3). 11. Optic nerve cupping Malpositioning of the lens is either the cause of 12. Tapetal hyperreflectivity the glaucoma (ie. anterior luxation) or a sequelae to buphthalmos induced zonular Diagnosis - Tonometry rupture (most subluxations). Cataract formation Establishing a definitive diagnosis can only and liquefaction of the vitreous (syneresis) are be through the measurement of the lOP. The fiequently seen associated with altered aqueous most routinely employed method of estimating dynamics. Ophthalmoscopic examination yields lOP in veterinary practice is digital tonometry. two commonly observed abnormalities. Cup­ Although this method elirrlinates the need to ping of the optic nerve head is seen clinically as purchase additional instrumentation, it is entirely truncated retinal vessels at the optic nerve head too insensitive to assess those subtle pressure which is not in the same plane of focus as the alterations occurring in early glaucoma sus­ remainder of the fundus (Fig. 4).Posterior pects. As such, digital tonometry cannot be mechanical displacement of the lamina cribrosa recommended for the recognition or manage­ with subsequent distortion of the laminar pores ment of glaucomatous eyes where retention of prevents the normal axoplasmic and hemody­ vision is the main objective. namic flow necessary for retinal viability. Instrumentation tonometry is generally Accompanying retinal degeneration is seen as divided into two distinct groups, indentation or tapetal hyperreflectivity, retinal vascular applanation tonometry. Both have their attenuation, and hyperpigmentation of the advantages and disadvantages. The Schiotz® tapetal fundus as pigment infiltrates from the indentation tonometer is the most widely adjacent retinal pigment epithelium (Fig. 4). purchased tonometer for veterinary practice. Eventually the diagnosis is obvious, but not until This instrument measures the amount of corneal vision has been irreversibly lost (Table 2). indentation achieved with the addition of a given, yet variable, amount of weight. Although very cost effective and accurate, this instrument Table 1 does posses a relatively large foot plate, thereby Clinical Signs of Acute Glaucoma making it more susceptible to the influences of 1. Lacrimation "scleral rigidity" or concurrent corneal pathology. 2. Photophobia One other drawback, especially when used in 3. Blepharospasm large animal practice, is that it must be used in a 4. Congestion of conjunctival/episcleral vertical orientation. Alternatively, applanation vessels tonometers have the advantages of a relatively 5. Corneal edema small foot plate and can be used in any orienta­ 6. Mydriasis tion. Compared to indentation units, these 7. Blindness instruments determine the amount of pressure 8. "Hard" eyes required to flatten or "applanate" the given area of cornea below their foot plate. Although numerous models are currently marketed, they are considerably more expensive than the Schiotz® tonometer, and usually are available only at referral centers. Vol 55, No.1 37 Diagnosis - Classification evaluation of the fellow eye helps to establish Once an elevation in lOP has been deter­ whether it is also at risk. Early surgical interven­ mined, classification of the glaucoma is essential tion in the fellow eye appears to significantly if the correct therapeutic approach is to be prolong normal lOP with subsequent retention of undertaken. Numerous classification schemes vision for these patients. In man the vast have been described to date. One of the most majority of primary