Cataracts, Dr. Christa Corbett, 11/8/14

cataracts, veterinarian

1. Christa Corbett, DVM, MS, DACVO
November 8, 2014

2. Outline
Anatomy of the lens
Nuclear sclerosis vs. cataract
Stages of cataracts
Etiologies of cataracts
When to refer
Pre-operativecare
Cataract surgery
Post-operative care
Medical treatment ???

3. Anatomy
AP
Zonules
Lens capsule
Nuclear vs. Cortical
Lens epithelium
Anterior
Produces new fibers
Equator
Active mitosis

4. Nuclear (Lenticular) Sclerosis
Lens continually produces
new cortical fibers
Compression of nucleus in
patients over 6-8 years old
Causes light to scatter
We can still see retina, patient
is still visual
Diagnosis:
DILATIONand RETROILLUMINATION
AP

5. RETROILLUMINATION

6. Stages of Cataract
Incipient -<10%
Minor opacities, often incidental
Perfect view of fundus

7. Stages of Cataract
Early immature –10-50%
Obvious opacity, but good tapetal
reflex and good view of fundus

8. Stages of Cataract
Late immature –51-99%
Can still see tapetalreflex, but very
limited view of fundus

9. Stages of Cataract
Mature –100%
No tapetalreflex on retroillumination

10. Stages of Cataract
Hypermature–resorbing
Varying degrees of lens opacity
Wrinkled capsule, “Sparkly” cataract

11. And other minutia terms that
Ophthalmologists love . . .
Morgagnian–subset of hypermature
Cortex resorbs, nucleus drops

12. And other minutia terms that
Ophthalmologists love . . .
Brunescence–Yellow!
Very old patients, very oldcataracts

13. And other minutia terms that
Ophthalmologists love . . .
Intumescence = FAT
Quick forming diabetic (occasionally
inherited)

14. Tendency to progress
Nuclear: rarely
progress
Cortical: variable,
often progress
(esp. anterior)
Equatorial: often
progress
AP

15. Etiology
Inherited
Diabetes
Senile
Trauma
Uveitis
Horses
Cats
Nutrition
Irradiation
Hypo/Hyper Ca
2+
Electrocution
Toxic
PRA
Drugs

16. Diabetes mellitus
Dogs only!
75% incidence within one year of onset of DM
Mechanism of action
Increased amount of glucose in the eye
Overloads the hexokinase pathway, so excess
glucose shunted into sorbitol pathway
○Enzyme Aldose Reductase is responsible for this
shunting
Sorbitol is too big to diffuse through the lens capsule
Osmotic gradient = more fluid pulled into lens
○Vacuolization of proteins
○Lens protein aggregation

17. Senile Cataracts
Refersto time of onset, and etiology
Very slow to progress
I do not have an age cut off, but I will
NOTdo surgery in an elderly dog if
there are signs of:
Cognitive dysfunction
Retinal degeneration
Significant corneal degeneration

18. When to refer
Do NOTlet the cataract “ripen!”
The earlier the better
It may be possible to get a view of theretina
in early cases
Start anti-inflammatory therapy before
problems arise
Clients can prepare themselves
and save money, take vacation
time, etc.

19. Sequelaeof cataracts if surgery
not performed early . . .
Loss of vision
Lens induced uveitis:
Cataractouslens proteins
leak out of lens uveitis
Lens capsule rupture
Lens luxation
Secondary glaucoma
Retinal detachment
Capsular mineralization

20. Treatment before referral
Anti-inflammatory therapy
If cataract is immature or beyond
Topicalsteroid
○PrednisoloneAcetate ($$$)
○NeoPolyDex
Topical NSAID
○Diclofenac
○Flurbiprofen
Quiet eye: SID-BID
Hyperemic, miotic, aqueous flare: TID-QID
○Consider an oral NSAID as well
Check bloodwork for diabetes
Monitor for glaucoma if possible

21. RetinalTesting
Outpatient testing, typically half-day
hospital stay
Sedationis rarely necessary
Retinal FUNCTION
Electroretinogram
Retinal STRUCTURE
Ocularultrasound

22. RetinalTesting

23. Artificial lenses
Placed inevery eye if possible
Cannotbe placed with:
Zonularinstability
○Risk of future lens luxation
Ruptured lens capsule
○Iatrogenic or pre-op (especially diabetics)
Hypermaturecataract with immense
capsular contraction = too small to hold a
lens

24. Artificial lenses
Rigid 
Polymethylmethacrylate(PMMA)
Requires an 8mm corneal incision
○More risk of astygmatismor incisionalleakage
Foldable
Acrylic 
Silicone
Folds into injection cartridge,
3mm incision

25. Suturing
9-0 monofilament absorbablesuture
(PGA, Vicryl®)
Smaller than a piece of my hair!
Suture pattern is surgeon-dependent
Double continuous, or “Shoe-lace”
9-0 vicryl
6-0 silk
Hair
E-collar is
MANDATORY!

26. Post-Operative Patient
Patients are immediately visual!

27. Successrates with surgery
85-95% success for most patients
Success rate decreases with:
○Hypermaturity
○Uncontrolled lens induced uveitis
○High or High-normal IOPs
Might be even lower % in certain breeds
○Bichon(Retinal detachment)
○Boston Terriers and Pugs (Glaucoma, corneal health)
○Shih Tzu (Corneal health)

28. Post-opOcular Complications
Common:
Fibrin
Refractory uveitis
Secondary glaucoma
Retinal detachment
Corneal ulceration
Posterior capsular opacity
Rare:
Artificial lens or capsular luxation
Hyphema
Endophthalmitis(sterile or bacterial)

29. Posterior Capsular Opacification
100% of dogs

30. Minimal PCO in most cases!

31. Hypermaturecataract leadingto
mineralized capsule plaques

32. Post-operative care
Enough eye drops to drive our clients crazy!
4-6 differentmedications, all QID
○Anti-inflammatory drops
Predacetate and Diclofenac
○Antibiotics
Somethingthat will penetrate the cornea = Fluoroquinolone
○Lubricant gel
Optixcaregel
○+/-Glaucoma drops
○+/-Dry eye meds (only ifpreviously diagnosed)

33. Post-operative care
Oral medications BID
Antibiotic(Clavamoxor Cephalexin)
Anti-inflammatory (Rimadyl)
E-collar!!!
24-7 for at least 2 weeks!
Warm compress the eyes to keep clean
of discharge

34. Post-operativecare
Rechecks:
+/-24 hours
+/-1 week
2 weeks –taper drops, remove e-collar
6 weeks
3 months
Every 4-6 months for LIFE!
○Every complicationlisted can happen even
years afterwards!

35. Rechecks–Primary care vet
vs. DACVO?
Every single recheck:
Schirmertear test
Intraocular pressure
Slit lampanterior exam
○Corneal health
○Grade of aqueousflare
○Grade of Posteriorcortical opacity (PCO)
○Lens position (subluxation, centrationof IOL)
Indirectfundicexam
○Retinal position –must look all the way out to the
oraciliarisretinae, most common area for detachments
to begin
○Signs of retinal hemorrhage
○Signs of subretinaledema
○Signs of vitrealdegeneration

36. Non-surgical patients
Topical NSAIDs for life (SID-BID)
Monitor IOP every3-4 months
Painful:
Glaucoma, uveitisand lens luxation
Non-painful:
Retinal detachmentand hyphema

37. Will medical treatment eliminate
cataracts?
Cataractogenesis
Denaturationof lens proteins
○Physical disruption of lens fibers
Trauma
○Altered osmotic gradients
Diabetes
○Oxidative damage
Aging
○Genetic predisposition

38. •Thirty dogs treated for at least 2 months
•Reduction of lens opacity in dogs with
immature cataract or nuclear sclerosis
•Owner reports “suggested” improved visual
behavior in 80% of cases

39. •In vitro
•Grapeseedextract
•Significant inhibition of mechanisms
of oxidative stress
•In vivo studies not yet presented
AJVR 2008

40. •Controlled study
•12 months
•Drop given TID OU
•Significant inhibition of
cataract when given at
time of DM diagnosis

41. Questions???