Secondary Glaucomas Flashcards
What is secondary glaucoma?
glaucoma caused by some other entity, characterized by site of aqueous obstruction
What are sites of aqueous obstruction?
pre-trabecular, trabecular, post-trabecular
What are pre-trabecular glaucomas?
neovascular, ICE syndrome and epithelial ingrowth
What are trabecular glaucomas?
hyphema, pigmentary, pseudoexfoliation
What are post-trabecular glaucomas?
episcleral venous pressure
What are other names for neovascular glaucoma?
hemorrhagic, congestive, thrombotic
What are main causes of rubeosis?
DM, retinal vascular occlusive disease, carotid artery disease, RD, sickle cell retinopathy, uveitis
What is 90 day glaucoma?
rubeosis in first 3 months after CRVO
Rubeosis mechanism:
ischemic retina, release of VEGF produced by muller cells, VEGF travels through pupil and over the iris and into the angle
NVG treatment:
treat underlying etiology in pre-angle closure stages, aka PRP or tx of carotid disease, use aqueous suppressants and filters/drainage devices, anti-VEGF
How does anti-VEGF work?
avastin injections showed excellent regression of NVI, good resolution of open angle NVG (still need some filtering), resolves neo in closed angle but IOP is not improved
Which medications reduce aqueous production?
alpha agonist, beta blocker, CAI
What is ICE syndrome?
iridocorneal endothelial syndrome- abnormal corneal endothelium forms membrane over angle
What are ICE demographics?
middle age female, possible association with HSV, EBV trigger, associated with progressive iris atrophy and cogan reese and chandler (most common)
What is the pathology of ICE?
collagenous layer bound to the posterior aspect of Descemet’s membrane, a cellular membrane develops over angle, yields synechiae further blocking the AC angle, cellular membrane on the iris
What is a corneal sign of Chandlers?
thickened endothelial layer
How is ICE diagnosed?
consider specular microscopy for better eval of corneal endothelial cells
What is the treatment of ICE?
topical aqueous suppressants, trabeculectomy, filtering procedures, PKP, descemet stripping automated endothelial keratoplasty, deep lamellar endothelial keratoplasty, descemets membrane endothelial keratoplast
What are characteristics of ICE?
sporadic, usually unilateral, W>M, 20-50 years old
What is epithelial ingrowth?
rare, post surgical or trauma, corena or conj grows into anterior chamber, epithelium of K or conj can get into wound and proliferate to block the TM, membrane covers angle
What are the surgical interventions for epithelial ingrowth?
remove/destruct epithelium or filtering procedure
How does a hyphema affect IOP?
less than 1/2 of AC filled= 4% incidence of IOP increase, greater than 1/2 of AC filled= 85% incidence of IOP increase
What is the etiology of hyphema induced glaucoma?
most commonly traumatic, post surgical
What is the therapy for hyphema?
stop anticoagulant/aspirin (consult PCP), rest no strenuous activity, upright posture, aqueous suppressants, topical steroid
What is the controversy of mydriasis as hyphema therapy?
may cause vasoconstrictive effect to reduce the persistence of a hyphema or pushing iris forward into angle which could potentially further narrow angle
When should you do a surgical anterior chamber wash?
with a total hyphema lasting more than 5 days
What is PDS?
bilateral pigment release from posterior iris, irido-zonular contact
Who is PDS more common in?
myopes and caucasians
What are signs of PDS?
Krukenberg spindle, pigment granules on iris, open angle with pigment/sampaolesi’s line, iris TID, sheie ring on anterior lens
What is the pathophysiology of PDS?
excessive pigment in angle causing IOP increase and ONH damage, IOP spikes with exercise
What are characteristics of PDS?
symptomatic in 40s, M>W, may be asymmetric
What is the PDS therapy?
miotics if tolerable, topical GLC med, PI, laser trabeculoplasty, trabeculectomy
What is the risk of pilo in PDS?
pilo stretches iris to pull it away form the lens zonules, there are SEs like accommodative spasm and risk of RD in high myopia
What is a good GLC med for PDS?
reduce production/alternative outflow, rho kinase inhibitors are good as they work at TM to open up the spaces and increase contractibility of TM
What is true of ALT and SLT in PDS?
pigment absorbs energy
What is pseudoexfoliative glaucoma?
extracellular material develops in anterior chamber clogging the TM
What are signs of PXE?
moth eaten pupillary ruff, bulls eye pattern on lens, flare appearance, corneal endo deposits possible, dandruff like debris on gonio
What does moth eaten pupillary ruff describe?
TIDs close to pupillary border
What is the hallmark sign of PXE?
bulls eye pattern on lens, iris starts to rub off the material on the lens so you see a bulls-eye appearance on the lens from iris constriction and dilation
What are characteristics of PXE?
Scandinavian descent, more females have the syndrome but more males have glaucoma as a result, genetic predisposition of LOXL1, 7th decade of life, unilateral/asymmetric, 20% with syndrome develop glaucoma
What is PXG therapy?
topical GLC meds, ALT/SLT, filtration sx, poorer prognosis than POAG due to fluctuations and IOP spikes/greater risk of treatment failures
What is not curative for PXG?
phaco IOL is not curative, you just don’t see deposition as readily due to not having deposition for a plethora of years
What is inflammatory glaucoma?
IOP spike with AC inflammation, may have initial low IOP due to CB dysfunction in inflammatory attack, WBC/RBC/debris in TM
What is the etiology of inflammatory glaucoma?
traceculitis
What does inflammatory glaucoma lead to?
PAS and PS
What are therapies for inflammatory glaucoma?
treat inflammation/disease (caution with steroid b/c IOP elevation possible), mydriasis, NO PGA, beta blocker or CAI or alpha agonist good, LPI, filtration surgery
Why is a LPI likely to close in inflammatory glaucoma?
due to inflammation and scarring
What are phaco glaucomas?
phacolytic and phacoantigenic
What is phacolytic?
high molecular weight proteins leak from lens with intact capsule and deposit in the angle, macrophages lodge in angle
What is phacoantigenic?
lens proteins leak through ruptured capsule, inflammatory response, post sx with retained material
What are signs of traumatic glaucoma?
disruption of angle structure/integrity, hyphema, angle recession
What is acute and long with angle recession?
acute: trauma can pull TM directly and damage schlemm’s canal to reduce outlfow// longterm: scarring of TM and schlemm’s causing later stage IOP elevation
What is the pathophysiology of traumatic glaucoma?
direct trauma to TM, debris in TM yield scarring, migration of endothelial cells over TM
What is treatment of traumatic glaucoma?
POAG more common in opposing eye, treatment with aqueous suppressants or filtration surgery
What is the typical episcleral venous pressure?
8-10 mmHg
What is the normal drainage process?
outflow requires a pressure gradient so an area of higher pressure can drain into an area of lower pressure, if EVP is elevated, we don’t have as much of a gradient so we get reduced outflow
What two things cause increased EVP?
carotid cavernous fistula and sturge weber syndrome
What is a carotid cavernous fistula?
abnormal communication of arterial and venous flow in cavernous sinus, increase pressure in sinus leads to poor venous drainage
What is the treatment of CC fistula?
surgical tx of fistula is high risk because it is in the middle of the brain, tx IOP with aqueous suppressants, if neo filtration procedure
What is sturge-weber?
phacomatosis, vascular hamartoma leading to increased EVP, may also have angle malformation
What is the most obvious sign of sturge-weber?
port wine stain along trigeminal distribution, noted at birth/early age
What is the glaucoma incidence with sturge-weber?
50% esp if ophthalmic and maxillary divisions are involved
What is the mechanism of sturge weber glaucoma?
anomalous development of angle, neo possible (requires goniotomy at young age to remove TM), small fistulas in episcleral vessles… if eyelid is involved glaucoma is more common
What is therapy for sturge weber glaucoma?
pharm therapy if later onset, filtration surgery often needed for younger patients esp with neo present
