Glaucoma Flashcards
describe the flow of aqueous humor
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
what are 6 causes of outflow obstruction that can result in pressure elevation?
- iridocorneal angle closure
- accumulation of proteoglycans in trabecular meshwork
- infiltration of ICA with inflammatory/neoplastic cells
- neovascularization of iris spanning angle
- synechiae:
-peripheral anterior
-posterior
-iris bombe - lens luxation/subluxation
how do we measure IOP?
- schiotz tonometry:
-applanation and rebound tonometry
-use tono-vet and tono-pen - normal is around 15-22mmHg but there is lots of variation on normal so we look at differences between eyes too
- 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)
describe applanation tonometry
- can only increase IOP with poor technique (no false low readings)
- easy mistakes:
-pressure on neck
-head position
-squinting dog
-pressure on globe from improper lid retraction
-tip cover not on properly
what is gonioscopy?
evaluation of the iridocorneal drainage angle with special lenses
what are clinical signs of glaucoma? (4)
- red eye, BIG pupil
- ciliary flush: deep corneal neovascularization; only indicative of intraocular disease though, a nonspecific sign
- optic nerve head cupping:
-due to mechanical “bowing” and atrophy/degeneration; retinal vessels disappear at the edge of the disc
-very negative prognostic indicator - optic nerve atrophy/degeneration:
-grey/dark pallor, loss of myelin/round
-cupping of optic nerve head
what are signs of chronic glaucoma?
- buphthalmos:
-enlarged globe due to stretching of cornea and sclera
-patient usually blind at this point; end stage sign - Haab’s stria:
-grey, curvilinear streaks in cornea
-breaks in descemet’s membrane from stretching of globe - lens subluxation:
-stretching of zonules from buphthalmia
-aphakic crescent: usually sign of irreversibly blind
describe primary versus secondary glaucoma
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!
describe prognosis for vision
- visual or with potential for vision:
-acute (<24-48 hours)
-positive menace, dazzle reflex, or consensual PLR to fellow eye
-normal optic nerve head - 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)
describe goals of glaucoma therapy
- save or regain and maintain vision
- 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
describe emergency therapy for primary glaucoma (3 most common, but 6 total)
- 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 - osmotic diuretics:
-mannitol IV or glycerin PO
-pull fluid out of cells, beware of heart disease, diabetes, renal failure, dehydration! - 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
- miotics/pilocarpine 2%:
-increase outflow
-irritating, exacerbates uveitis - anti-inflammatories
- beta blockers:
-decrease aqueous production
-timolol 0.5%, betaxolol 0.5%
-systemic administration may be neuroprotective
describe long term therapy for primary glaucoma
- medical therapy will usually fail within a year, as none of it fixes the broken drain (iridocorneal angle)
- 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 - 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 - but usually end up with double enucleation
describe prophylactic therapy of the fellow eye in a case of primary glaucoma
- betaxolol/timolol 0.5% with steroid
-may be associated with increased incidence of KCS
OR
- dorzolamide BID or TID OR
- 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
describe secondary glaucoma due to uveitis
- obstruction of filtration apparatus as inflammatory cells/fibrin accumulate in IC angle
- beware normal IOP with uveitis, could still be obstruction of angle-debris, cells, and pre-iridial fibrovascular membrane
- 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
describe treatment of secondary glaucoma due to uveitis
- aggressive therapy for uveitis
-topic steroids and NSAIDs
-systemic steroids after diagnostics - AVOID miotics (latanoprost) and mannitol
- can use topical carbonic anhydrase inhibitors, beta-blockers
- long term prognosis for vision usually poor due to irreversible scarring
