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Glaucoma Paul E. Miller, DVM, Diplomate ACVO University of Wisconsin-Madison GLAUCOMA: A diverse group of diseases united by a common theme in which IOP is too high for the optic nerve to function properly resulting in the loss of some or all vision Incidence VMDB over 20 years

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glaucoma
Glaucoma
  • Paul E. Miller, DVM, Diplomate ACVO
  • University of Wisconsin-Madison
slide3

GLAUCOMA: A diverse group of diseases united by a common theme in which IOP is too high for the optic nerve to function properly resulting in the loss of some or all vision

incidence
Incidence
  • VMDB over 20 years
  • 1 in 119 dogs
  • 1 in 367 cats
  • Screening cats > 7 years old
  • 1 in 111 cats
intraocular pressure
Intraocular Pressure
  • Inflow = Outflow
  • Production
    • Active Secretion – Energy – 70%
      • NaK pump
      • H20+ CO2H2CO3 HCO3- + H+
    • Diffusion – Lipid soluble
  • Outflow
    • Trabecular Meshwork – Most
    • Uveoscleral – 3-15% to 50%
    • Via Iris
  • Glaucoma is almost always due to impaired outflow
slide7

Step 1: Impaired Outflow  Increased IOP

  • Apoptotic triggers include:
    • Neurotrophin deprivation - Excess glutamate
    • Apoptic gene activation - Ischemia
    • Excess nitric oxide - Free radicals
    • Lipid peroxidation - Autoimmunity
    • Helicobacter pylori infection
  • A vicious cycle may then result

Step 2: Ischemia/Deformation

Step 3: Necrosis Apoptosis

diagnosis tonometry
Diagnosis - Tonometry
  • Indentation - Schiøtz
  • Use human calibration tables

Original Schiøtz

diagnosis tonometry13
Diagnosis - Tonometry

Applanation – Tono-Pen

slide14

Diagnosis - Tonometry

  • Induction-Impact (Tono-Vet)
    • Species specific calibration
    • No topical anesthesia
    • Accurate in normal dogs and horses
    • Unsure accuracy in disease
diagnosis gonioscopy

Koeppe

Diagnosis - Gonioscopy

Lovac

eyevetclinic.co.uk

PLD – Sheets/flow holes

Open

Slightly Narrow

Closed

evaluation schemes
Evaluation Schemes
  • Ekesten AJVR 1991

Width and pectinate ligament dysplasia may be separate entitites

slide17

Glaucoma Classification

Primary

- Open-angle

- Angle-closure

- Congenital

Secondary

- Lens associated

- Uveitis

- Hyphema

- Neoplastic

- Post-surgery

- Many others

slide20

PACG Risk Factors

  • Mid/older age • Stress
  • Dim light/night • Genetic
  • • Mid-range pupil • Abnormal angle
  • Females 2:1

http://www.aacca.net/newsletterimages/old116.jpg

slide21

Normal

Sheets and flow holes

Sheets

Goniodysgenesis

(Pectinate Ligament Dysplasia)

how pacg develops dogs
How PACG Develops - Dogs

Normal

PACG

PLD is only first “hit”

slide24

GLAUCOMA

VISUAL

VISUAL OR BLIND ?

BLIND

Determine primary cause

Relieve pain

Enucleation

Evisceration / prosthesis

Cyclocryosurgery

Cyclophotocoagulation

Evaluate fellow eye

PRIMARY OR SECONDARY ?

PRIMARY (CLOSED)

Medical Therapy

0.005% Latanoprost

or if ineffective

Mannitol

2% Pilocarpine

Methazolamide

Recheck IOP in 3-4 hrs

Evaluate Fellow Eye

SECONDARY

Treat 1o Cause

Uveitis

Lens Luxation

Hyphema

Neoplasia

Evaluate Fellow Eye

Prophylactic Therapy

Demecarium or Betaxolol

IOP q1 mo for 3 mo

then q 3 mo

IOP > 20

Perform Surgery

IOP < 20

Continue Medical Rx

Either Sx now or if

IOP > 20 mm Hg

Surgery

Combined Procedures

Cyclocryosurgery

Cyclophotocoagulation

Gonioimplantation

pgf 2 derivatives

37 mm Hg, PD: 8.0 mm

13 mm Hg, PD: 2 mm

PGF2 Derivatives
  • Highly species and dose specific
    • Are current “front-line” drugs in humans
    • Xalatan doesn’t work in cats
  •  uveoscleral outflow ( traditional)
  • Can  aqueous production in dogs
  • Intense miotic in animals
  • Can  IOP 50+ mm Hg
pgf 2 derivatives26

PGF2

Unoprostone

0.12%Rescula® Novartis

Latanoprost

0.005% Xalatan® Pfizer

Bimatoprost

0.03% Lumigan® Allergan

Travoprost

0.004%Travatan® Alcon

PGF2 Derivatives
  • Latanoprost best studied
  • All work  same
  • Are additive to all other anti- glaucoma drug classes:
  • BUT: Pilocarpine may reduce efficacy
  • NSAIDS don’t directly interfere
    • BUT: Topical PG’s may recruit endogenous PGs to further IOP
hyperosmotics
Hyperosmotics
  • Osmotic gradient dehydrates vitreous
  • Big drop (50-60 mm Hg) in 1-2 hrs
  • Short-lived effect (1-2 days)
  • Toxicity limits to potentially visual eyes
  • BAB breakdown relative contraindication
  • Not in CHF (both) or DM (glycerin)
  • Additive to all other anti-glaucoma drugs
  • 1st choice only in pre-op lens luxation
  • Now 2nd to PGs in acute PACG
carbonic anhydrase inhibitors
Carbonic Anhydrase Inhibitors
  •  aqueous humor production
  • Systemic toxicity – acidosis, K+, panting, vomiting, diarrhea, weakness
  • Systemics being replaced by topicals ( toxicity)
  • TID topical  BID systemic after 1 week (dog)
  • 20-30% IOP 
  • Maintains IOP lowering ability over time
  • Often use with a hyperosmotic in acute PACG
  • First choice in many secondary glaucomas
  • Additive to all other classes
topical cais
Topical CAIs
  • Irritation primary side effect
  • Dorzolamide 2% (Trusopt®, Merck)
  • Cosopt®(Merck) = dorzolamide plus timolol
  • Brinzolamide 1% (Azopt®, Alcon)
cholinergics
Cholinergics
  • Old (1873) but potent class
  • 3rd choice to PGs and CAIs in most
  • Increase outflow via TM
  • Contracts longitudinal ciliary muscle
  • Miosis reopens angle/break pupil block
  • Additive to every class (+/- PGs)

Pilocarpus pennatifolius

adrenergic agonists
-Adrenergic Agonists
  • Been used for 50+ years
  • 2nd choice to CAIs in some secondary glaucomas
  • Usually in combination in primary glaucomas
  • Epinephrine 1-2% q6-12 hrs
  • Dipivefrin0.1% BID
  • Pro-drug cleaved in AC  irritation
  • 10X IOP lowering effect of epinephrine
  • May  outflow via ß-2 receptors in TM
  • May  uveoscleral outflow (relax CB, recruit PGs)
    • NSAIDS may partially block
  • May  or  aqueous production
  •  efficacy with time
  • Adverse effects: Irritation
adrenergic blockers
-Adrenergic Blockers
  • First-line prior to PGs in humans
  • Inhibit ß- 2 receptors on ciliary epithelium  aqueous production
  • 3rd choice in some secondary glaucomas or as prophylactic
  • Only mild  in animals – sleep/receptors
  • May outflow dogs/cats (miosis)
  • Additive to other classes except  agonists
beta blockers
Beta Blockers
  • Timolol maleate 0.5% q12hr
    • Non-selective -1 and -2 blocker
    • Bradycardia possible
    • May worsen asthma (cats)
    • Potent miotic (dog/cat)
  • Betaxolol HCL 0.5% q12hr
    • Cardioselective (-1)  risk in asthma
    • <IOP than timolol
    • Recently shown to be neuroprotective
    • Mild miosis
    • Proven PACG prophylactic
  • Other -1/-2
  • Metipranolol, Levobunolol,Carteolol
glaucoma drug therapy compliance
Glaucoma Drug TherapyCompliance

Human anti-glaucoma drug compliance

pacg other forms
PACG – Other Forms
  • Latent - “at risk” fellow eye
  • Intermittent – attacks that spontaneously resolve
  • Acute congestive – sudden attacks that don’t resolve
  • Post congestive – had an attack but now normal IOP
  • Chronic – gradual increase
  • Absolute – end stage
latent form
Latent Form
  • “Normal” fellow eye
  • At high risk – 50% in 8 months
  • Abnormal angle/S-shaped iris
  • Cleft open initially – may close later
  • Preventative drops lower risk to 50% in 30+ months

Possible Course

intermittent form
Intermittent Form
  • 8-yr-old FS Cocker Spaniel
  • Vague Hx transient red eye at night or with child crying
  • PLD OU
  • R L
  • 8AM 15 17
  • 9AM 13 21
  • 11AM 16 23
  • 1PM 17 41
  • 2PM (latano) 16 12
  • Cleft Closed on HRUS
intermittent pacg course
Intermittent PACG - Course
  • Remain normal – rare
  • Develop acute PACG – most common
  • Develop chronic PACG - occurs
slide45

GLAUCOMA

VISUAL

VISUAL OR BLIND ?

BLIND

Determine primary cause

Relieve pain

Enucleation

Evisceration / prosthesis

Cyclocryosurgery

Cyclophotocoagulation

Evaluate fellow eye

PRIMARY OR SECONDARY ?

PRIMARY (CLOSED)

Medical Therapy

0.005% Latanoprost

or

Mannitol

2% Pilocarpine

Methazolamide

Recheck IOP in 3-4 hrs

Evaluate Fellow Eye

SECONDARY

Treat 1o Cause

Uveitis

Lens Luxation

Hyphema

Neoplasia

Evaluate Fellow Eye

Prophylactic Therapy

Demecarium or Betaxolol

IOP q1 mo for 3 mo

then q 3 mo

IOP > 20

Perform Sx

IOP < 20

Continue Medical Rx

Either Sx now or if

IOP > 20 mm Hg

Surgery

Combined Procedures

Cyclocryosurgery

Cyclophotocoagulation

Gonioimplantation

feline glaucoma
Feline Glaucoma

Uveitis induced

LSA

Melanoma

FAHMS

drug therapy summary
POAG: PG, CAI,  blocker

PACG: PG, Hyperosmotic, CAI, cholinergic, ±  agonist

± blocker

Prophy: Cholinergic, PG,  blocker

Uveitis: CS, NSAIDS, CAI, ±  agonist ± blocker

Hyphema: CS, CAI, ± cholinergic, ±  agonist, ± atropine

Lens Lux: CAI, ± Hyperosmotic ± PG, ± cholinergic,

±  agonist, ± atropine

Neoplasia: Chemotherapy, CAI, no outflow

FAHMS: CAI,  agonist

Drug Therapy - Summary
slide53

Future Therapy: Neuroprotection

DamageRepairHealth

(stress proteins, growth factors

anti-apoptosis compounds)

(NO synthase inhibitors)

GlutamateCalcium Nitric Oxide

(glutamate blockers)

(calcium blockers)

(Anti-oxidants)

(stress proteins)

Free Radicals Death

Note: These are many of the same issues in other neurodegenerative disorders and so therapies for those disorders may be applicable to glaucoma therapy

memantine
Memantine
  • NMDA glutamatergic open-channel blocker
  • Blocksexcitotoxic cell death
  • vision loss even if IOP remains high
  • Approved in Europe
  • Alzheimer’s and Parkinson’s
  • Few side effects
  • Likely additive to all classes