Module 8 Flashcards
Glaucoma
How is aqueous produced? Where? What causes glaucoma?
Physiological control of IOP
Constant production and drainage.
Aqueous, from non-pigmented epithelium of ciliary body. 80% active, 20% by diffusion and ultrafiltration.
Active: CO2 + H2O –> (catalyse by carbonic anhydrase) H2CO3 –> HCO3- + H+
Movement of bicarbonate ions into the posterior chamber creates osmotic gradient, water from ciliary stroma moves into posterior chamber as well.
Hence, how carbonic anhydrase inhibitors drop IOP
Junction of base of iris and corneoscleral tissue = iridocorneal angle which includes drainage apparatus; the pectinate ligaments and ciliary cleft (full of trabecular meshwork tissue) = conventional drainage
Unconventional drainage = uveoscleral outflow
IOP only increases in glaucoma as a results of increased outflow resistant, not from hypersecretion of aqueous.
Normal variations in IOP
RR 15-25mmHg Variations: -instrumentation used -age of dog; may decrease with age -Head position; head up or dorsal recumbency ^IOP -Restraint; vigorous may ^ IOP -Forced lid opening; ^IOP -Breed; terriers, fluctuant IOP -Obesity and A-BP
Gonioscopy required to asses drainage angle in dogs, not required for cats. Not dilated and LA applied.
Glaucoma; “The Glaucomas”
Glaucoma = increased IOP –> damage to retina and ON that results in total irreversible blindness.
A complex of several separate entities. Prolonged elevated IOP in our species. Humans have a form of normotensive glaucoma. Most profound damage is on ONH with ganglion cells –> visual field loss.
Clinical signs. Acute. Dogs only.
Pain - nociceptors in cornea and globe. Behavioural changes. Ocular signs; blepharospasm, photophobia, increased lacrimation.
Corneal oedema - endothelial pumps actively transports solutes out of the stroma into the aqueous. ^IOP interferes with this and the excess water disrupts the stromal lamellae. Less marked in lower IOP, chronic cases and cats. Deep corneal vessels - brush border may be seen, especially secondary to uveitis.
Mydriasis - pressure induced paresis or paralysis of iris sphincter muscle, moderate to dilate pupil. In some cases pupil may be constricted.
Episcleral congestion - common feature, engorged vessels run at right angles to the limbus, do not move when conj moved. Not all cases of episcleral congestion = glaucoma as can also occur in uveitis/panopthalmitis, episcleritis, retrobulbar-space occupying lesions.
Vision loss - ONH damage results in loss of vision. Second eye is usually starting to be affected by time of presentation. Os rarely notice unilateral blindness but signs include:
-Loss of menace in affected eye
-loss of dazzle response to bright light
-loss of consensual and direct PLRs
-absence of tracking response to cotton-wool ball (patch eye not being tested)
-inability to negotiate a maze (patch other eye)
In early stages vision loss could be reversible, but once >few days or very high IOP then prospects poor.
Chronic glaucoma. Dogs and cats.
Uncontrolled acute glaucoma or insidious onset presenting at point of irreversible damage. Pain and corneal oedema tend to be less obvious. In addition to acute glaucoma signs you can see:
- Neovascularisation from limbus, superficial arborising pattern, pigment deposition secondary to this.
- Globe enlargement from stretching of the ocular tunics, marked in young animals. Differentiate from exophthalmos - which is normal globe pushed forward. Exophthalmos see TEL prominence. Hydrophthalmos see TEL pushed in medial canthal region.
- Descemet’s fracture or Haab’s striae seen as greys streaks
- Lens luxation due to zonular fibre rupture. Must establish if lens luxation is cause or effect of glaucoma
- Cupping of optic disc - ONH bowed backwards through cribriform plate (a perforated region of sclera which allow ON to leave the globe). Best seen with bionocular indirect ophthalmoscopy.
- Cataract - chronic and lens luxation and probably results from alterations in nutrition of the lens
- IO haemorrhage
- Iris atrophy - retroilluminates or holes in iris. Can also be a senile change or as a sequel to uveitis
- retinal and ONH atrophy - end stage. loss of vasculature–> ONH chalky appearance, in dog may also grey with loss of myelinated nerve fibres. Retina - hyperreflective, retinal thinning and retinal vasculature attenuation.
- equatorial staphylomas - scleral thinning and stretching, outward protrusions.
- Phthisis bulbi - previously increase IOP, pressure-induced atrophy of the ciliary processes, aqueous production drops and in extreme cases phthisis bulbi and reduction of globe size.
Classification of glaucoma
Primary (no antecedent ocular dz) or secondary (following other ocular dz). Congenital also seen rarely.
Primary: hereditary basis:
PLA: ECS, Welsh and English SS, Basset Hound, Siberian Husky, Retrievers - Lab and golden, Welsh Terrier, ACS, Great Dane, Flat-coated retriever, Hungarian Viszla, Dandie Dinmont terrier, Border collie
Open angle glaucoma: Norwegian elkhound, petit basset Griffon Vendeen, Basset Hound
Pectinate ligament abnormality/goniodysgenesis
Most common form of primary glaucoma in the UK. PLA - ligament is abnormal and made up of mesodermal sheets with perforations by intermittent flow holes. May also be narrowed. In early life sufficient drainage and normotensive. Middle ages dogs, see compromise and acute glaucoma develops.
Ciliary cleft examined with 50MHz US in studies for more info.
Not strictly congenital as now found can progress with age.
Open-angle glaucoma
Open angle in dogs prove to be a good models for the disease in humans.
Not fully understood but suggestive of glycosaminoglycans build up in the drainage system. DNA tests are available for some breeds.
Drainage angle is normal on gonio
Secondary glaucoma
Most common glaucoma seen. Cats as well as dogs. Primary dz impairs drainage of aqueous at pupil or drainage apparatus.
Blockage at pupils: lens, vitreous, total posterior synechiae/iris bombe
Blockage at drainage apparatus: inflammatory cells, fibrin/haemorrhage, tumour cells, pre-iridial fibrovascular membranes (PIFMs), peripheral anterior synechiae, iris swelling, vitreous.
Secondary glaucoma - primary lens luxation
Terrier breeds + Border collie (to lesser degree)
Anterior lens luxation with vitreous prolapse can block both sites! Rapid rise in IOP.
Can also be seen with posterior lens luxation but less common.
Lens luxation - cause of effect of glaucoma?! Careful clinical assessment and hx taking. DNA tests for many terrier breeds
Secondary glaucoma - Uveitis
Mechanisms:
- infiltration of PL and ciliary cleft with inflammatory debris
- swelling of the trabecular meshwork
- swelling of the iris reducing drainage angle
- synechiae anterior and posterior (posterior adhesions between iris and lens –> iris bombe due to aqueous build up behind the iris)
- pre-irdial fibrovascular membranes
Secondary glaucoma - neoplasia
Mechanisms:
- neoplasia directly involved in the drainage structures
- accumulation of cells blocking ciliary cleft
- development of uveitis
- angiogenic factors –> neovascular tissue growth over PL (pre-iridal fibrovascular membranes)
Uveal melanoma, primary ciliary body adenoma/adenocarcinoma, lymphoma.
Dx can be difficult if glaucoma, full dx investigation, enucleation may be only way to achieve definitive dx
Secondary glaucoma - IO haemorrhage
Causes:
- trauma, IO neoplasia, uveitis, bleeding disorders, congenital lesions
Blood and fibrin clots compromise outflow. Haemorrhage may be effect rather than cause of glaucoma
Secondary glaucoma - ocular melanosis/pigmentary glaucoma
Cairn terriers accumulate pigment in the anterior segment
insidious onset glaucoma in middle-aged and older dogs.
Large amounts of pigment in anterior chamber, especially ventrally
Sporadically in other breeds - Golden retriever and WHWT.
Secondary glaucoma - Intumescent cataract
lens swelling can cause glaucoma due to effects on aqueous dynamics.
Lens induced uveitis is a more common cause of glaucoma due to leakage of lens material from hypermature cataracts
Secondary glaucoma - Vitreous prolapse
after IO surgery e.g. lendectomy or lens luxation
Obstruction to aqueous flow at pupil or at drainage apparatus. vitreal liquefaction - ageing process, can allow anterior movement of the vitreous.
Management of glaucoma
Medical or Sx, reduced IOP by decreasing production or increasing outflow
Factors to considers: duration of dz, degree of vision, underlying cause, gonioscopic findings, one-eyed case, age of patient, temperament of pt, finances
Management of glaucoma - medical
- ANALGESIA; NSAIDs +/- opiates
- Osmetic diuretics; acute cases with pressure >50mmHg. 1-2g/kg IV over 30 mins. Lasts few hours
- CAI; decrease aqueous production, 50% drop in IOP. No longer use systemic CAIs due to SE and topicals available. Dorzolamide and Brinzolamide. Dorzolamide has been shown to lower serum K+ in cats, monitoring K+ advised.
- Prostaglandin analogues; PGF2a - increase outflow via unconventional uveoscleral outflow, pronounced miosis, in an emergency used every 15 minutes for 4-6 doses but not in cases of uveitis or lens luxation. Latanoprost, travaprost, bimatoprost. Do not work in cats
- miotics; POAG, opens up trabecular meshwork, rarely used in our pts
- B-adrenergic blockers; reduce cAMP in ciliary processes. Increase outflow and combined with other drugs (e.g. dozolamide and timolol in cosopt). Timolol maleate, Betoxalol.
Management of glaucoma; Sx treatment of glaucoma
Methods to increase outflow: filtration devices. Shunted into subconjunctival tissue space. Thin piece of tubing, +/- valve and base plate. Tubing enter anterior chamber through a scleral tunnel. Aqueous is drained into tenon’s space. Scarring and fibrosis can occur after sx. Mitomycin C or 5 fluorouracil or beta-irradiation can improve this. Additional shunts also possible.
Methods to reduce aqueous production:
- cyclocryoablation; trans-scleral freezing of portions of ciliary body, visual or blind glaucomatous eyes, post-op spike in IOP, liquid nitrogen or nitrous oxide via 3mm probe, UGA, 4-8 sites 4-5mm posterior to limbus, sparing posterior ciliary arteries at 9 and 3 positions. Applied until “ice-ball” reaches corneal periphery (2 minutes). Superseded by laser.
- cyclophotocoagulation; as above but destruction with laser energy. Nd-YAG laser and diode are used. Low energy direct contact methods less complications cf. non-contact methods but less effective. Laser applied to 30-40 sites 3-4mm posterior to limbus, avoiding 9 and 3 positions. 1.2 W for 1.2 seconds. 50J per eye. Every 4th application an audible pop noise is heard due to vaporisation of fluid. Spikes post treatment common - paracentesis in eyes with potential for vision. Medical treatment 4 weeks post tx before attempt to reduce dose and frequency of CAI.
Management of glaucoma; Sx treatment of glaucoma - pharmacoablation
Pharmacoablation for blind eyes:
- gentamicin injected into the vitreous to destroy ciliary body and retina.
- UGA 0.5ml of vitreous is aspirated through sclera and 25 mg of gentamicin is injected.
- feline post-traumatic sarcoma in cats
- intractable uveitis may be seen, severe phthisis bulbi and may necessitate enucleation
Management of glaucoma; Sx treatment of glaucoma; Enucleation
Primary glaucoma - must be warned that other eye will follow
Bumper bars, echolocation used in some animals, most adjust within a few weeks and benefit from being pain free without frequent medication
Feline Glaucoma
Cats - deep chamber, allows gonio without a lens, and has a wide iridocorneal angle.
PLs - slender, widely separated, unbranching, gold/blue/white depending on iris colour
Glaucoma relatively uncommon in cats
RR 22.2 +/- 5.2mmHg
Hereditary predisposition Siamese and Persian, only proven in Lab strain of Siamese in the US. Few cases occur in absence of other ocular disease, older cats but uncommon
Majority are secondary..
- Uveitis - most common
- neoplasia - melanoma and lymphoma
- trauma
- lens rupture
- lens luxation - large anterior chamber so can have anterior lens luxation w/o ^IOP
- aqueous misdirection syndrome
Glaucoma is usually insidious and chronic in cats. Blepharospasm and lacrimation may be noted in the early stages, pain rarely exhibited. Mydriasis often presenting complaint. Conjunctival and episcleral congestion - red eye, to lesser extent cf. dog. Corneal oedema and bullous keratopathy in longstanding cases. Hydrophthalmos common, may lead to exposure keratopathy. Cataract and lens luxation due to stretching and breakdown of zonular fibres may occur. Retinal degeneration and ONH cupping and atrophy.
Aqueous misdirection; aqueous flows into vitreous causing it to swell and lens-iris diaphragm moves anteriorly. Closes ciliary cleft, ^IOP. Vitrectomy with lens removal is the most successful long term management.
Unilateral or bilateral. Tx difficult. Presented late with advanced and irreversible vision loss. Also primary condition needs to be managed.
Uveitis - CCS and other anti-inflammatory agents. Miotics are of little use in cats. CAI & beta blockers are useful in cats. PGF2a - will use miosis but not reduce IOP
Congenital glaucoma in cats: buphthalmos, uni or bi. Grossly enlarged globe with intense corneal oedema. Presumed catastrophic developmental abnormalities preventing drainage. Young animals - pronounced scleral stretching.
