Glaucoma

Question 1

describe the flow of aqueous humor

Answer 1

produced by the ciliary body and released into the posterior chamber where it then flows through the pupil to the anterior chamber and drains at the iridocorneal angle

normally aqueous humor production matches outflow

glaucoma occurs due to decreased AH outflow, obstruction of which results in elevation of IOP, which results in ischemia and deformation, which can lead to necrosis and apoptosis

Question 2

what are 6 causes of outflow obstruction that can result in pressure elevation?

Answer 2

1. iridocorneal angle closure
2. accumulation of proteoglycans in trabecular meshwork
3. infiltration of ICA with inflammatory/neoplastic cells
4. neovascularization of iris spanning angle
5. synechiae:
   -peripheral anterior
   -posterior
   -iris bombe
6. lens luxation/subluxation

Question 3

how do we measure IOP?

Answer 3

1. schiotz tonometry:
   -applanation and rebound tonometry
   -use tono-vet and tono-pen
2. normal is around 15-22mmHg but there is lots of variation on normal so we look at differences between eyes too
3. tono-pen:
   -flattens a circle of the cornea
   -displays an average; lowest repeatable is accurate
   -good for diseases corneas, works in any position
   -okay without topical anesthesia (but still probs just numb anyway)

Question 4

describe applanation tonometry

Answer 4

1. can only increase IOP with poor technique (no false low readings)
2. easy mistakes:
   -pressure on neck
   -head position
   -squinting dog
   -pressure on globe from improper lid retraction
   -tip cover not on properly

Question 5

what is gonioscopy?

Answer 5

evaluation of the iridocorneal drainage angle with special lenses

Question 6

what are clinical signs of glaucoma? (4)

Answer 6

1. red eye, BIG pupil
2. ciliary flush: deep corneal neovascularization; only indicative of intraocular disease though, a nonspecific sign
3. optic nerve head cupping:
   -due to mechanical “bowing” and atrophy/degeneration; retinal vessels disappear at the edge of the disc
   -very negative prognostic indicator
4. optic nerve atrophy/degeneration:
   -grey/dark pallor, loss of myelin/round
   -cupping of optic nerve head

Question 7

what are signs of chronic glaucoma?

Answer 7

1. buphthalmos:
   -enlarged globe due to stretching of cornea and sclera
   -patient usually blind at this point; end stage sign
2. Haab’s stria:
   -grey, curvilinear streaks in cornea
   -breaks in descemet’s membrane from stretching of globe
3. lens subluxation:
   -stretching of zonules from buphthalmia
   -aphakic crescent: usually sign of irreversibly blind

Question 8

describe primary versus secondary glaucoma

Answer 8

primary: angle closure; no other ocular abnormalities
-cockers, bassetts, chows

secondary: uveitis most common
-needs work up for uveitis
-often other eye affected too
-treat primary cause!

Question 9

describe prognosis for vision

Answer 9

1. visual or with potential for vision:
   -acute (<24-48 hours)
   -positive menace, dazzle reflex, or consensual PLR to fellow eye
   -normal optic nerve head
2. irreversibly blind:
   -chronic (>72 hrs)
   -buphthalmic (except puppies)
   -absent dazzle reflex, no consensual PLRs to fellow eye
   -grey/dark, round and cupped optic nerve head

if vision is possible, treat aggressively with the consideration of referral
if no vision possible, perform salvage procedure (enucleation or evisceration with intrascleral prosthesis)

Question 10

describe goals of glaucoma therapy

Answer 10

1. save or regain and maintain vision
2. achieve and maintain comfort via control of intraocular pressure at a target safe level (as close to 20 as can get)
   -avoid progressive optic nerve and retinal damage with associated visual deficits

Question 11

describe emergency therapy for primary glaucoma (3 most common, but 6 total)

Answer 11

1. topical prostaglandin derivatives/latanoprost 0.005%:
   -increase uveoscleral outflow, potent miotics
   -often results in decreased IOP in 1-2 hours
   -has mostly replaced mannitol and CAIs as emergency intervention
2. osmotic diuretics:
   -mannitol IV or glycerin PO
   -pull fluid out of cells, beware of heart disease, diabetes, renal failure, dehydration!
3. carbonic anhydrase inhibitors (CAIs)
   -include methazolamide, dorzolamide (topical), brinzolamide (topical)
   -carbonic anhydrase is key to AH production
   -be ware of hypokalemia, metabolic acidosis, PU/PU, V/D, confusion, and more

above are most common but also have

4. miotics/pilocarpine 2%:
   -increase outflow
   -irritating, exacerbates uveitis
5. anti-inflammatories
6. beta blockers:
   -decrease aqueous production
   -timolol 0.5%, betaxolol 0.5%
   -systemic administration may be neuroprotective

Question 12

describe long term therapy for primary glaucoma

Answer 12

1. medical therapy will usually fail within a year, as none of it fixes the broken drain (iridocorneal angle)
2. referral surgery:
   -gonioimplant: aqueous drainage, fails in 4-6 months
   –tube into AC, drains to footplate, then into subconjunctival space, expensive and fibrosis leads to early failure
   -cyclodestruction: laser or freeze, endoscopic or external; post op IOP spike can blind
   -combine the above, 50% success for vision at 1 year
3. prophylactic therapy:
   -if primary then good eye will likely also be lost in a median of 8 months but with therapy the median time to onset of glaucoma is 33 months
4. but usually end up with double enucleation

Question 13

describe prophylactic therapy of the fellow eye in a case of primary glaucoma

Answer 13

1. betaxolol/timolol 0.5% with steroid
   -may be associated with increased incidence of KCS

OR

2. dorzolamide BID or TID OR
3. demarcarium bromide 0.125% with steroid
   -may cause uveitis
   -salivation, vomiting, diarrhea, sweating, organophosphate toxicity (flea products)

-do NOT use latanoprost prophylactically
-steroids may have a long term benefit
-check IOP monthly for 3 months then every 3 months after that
-equip clients with an emergency kit with a prescription for latanoprost

Question 14

describe secondary glaucoma due to uveitis

Answer 14

1. obstruction of filtration apparatus as inflammatory cells/fibrin accumulate in IC angle
2. beware normal IOP with uveitis, could still be obstruction of angle-debris, cells, and pre-iridial fibrovascular membrane
3. iris bombe: 360 degree posterior synechiae causes aqueous humor to be trapped behind the pupil where the iris balloons out like a donut of bundt pan

Question 15

describe treatment of secondary glaucoma due to uveitis

Answer 15

1. aggressive therapy for uveitis
   -topic steroids and NSAIDs
   -systemic steroids after diagnostics
2. AVOID miotics (latanoprost) and mannitol
3. can use topical carbonic anhydrase inhibitors, beta-blockers
4. long term prognosis for vision usually poor due to irreversible scarring

Question 16

describe secondary glaucoma due to anterior lens luxation

Answer 16

1. movement of lens into anterior chamber
   -due to lens instability from breakdown of zonules
2. can be inherited in terriers, shar pei, english springer spaniels or secondary to cataract, chronic uveitis, trauma
3. obstructs the pupil +/- IC angle
4. this is the only type of glaucoma where you might dilate the pupil to relieve pressure

Question 17

describe secondary glaucoma due to neoplasia

Answer 17

1. neoplastic cells accumulate in IC angle
2. tumor obliterates IC angle