Optic neuropathy having increased IOP as main risk factor
Angle anatomy , vitreous volume is constant, aquous is variable, aqueous circulation, from non pigm. Ciliary processes …. Episcleral veins
POAG: symp.: asymp. Sight thief (screening) ,bilat. Male or female > 50 ,Sometimes headache, late field defects
Signs: high IOP, angle opened, fundus : cupping > 0.3, nasal shifting, stippling
Ttt: target IOP 20- 30 % less than initial
Start medical : PG once or BB twice , others : pilocarpine and alpha agonists
If failed : SST
Symp.: blepharospasm, lacrimation and late blue sclera and large globe
Signs: pseudoproptosis, large cornea , horiz. Haab’s stria, deep AC , IOP less than expected , fundus reversible cupping
Complic.: corneal edema heals by scar, lens sublax., amblyopia and nystagmus, optic atrophy
Exclude RB : fundus or B- scan
Ttt: clear cornea: goniotomy, opacity: trabeculotomy if failed SST
Patho.: hypermetropic female with shallow AC, angle becomes occluded by iris root ppt. by darkness and drugs
Symp.: severe pain up to vomiting, DOV
Previous intermittent attacks of headache and blurring
Signs: ciliary congestion ( blockade of venous drainage) , corneal edema, shalloe AC, semi dilated irreactive pupil, IOP stony hard
Ttt: decrease IOP by mannitol 20 % then YAG or SST acc to PAS > or < 50 % and prophylaxis to other eye
Etiology: severe chronic retinal ischemia
CRVO mc, DM, intraocular tumor, long standing retinal detachment
Ttt: avoid pilocarpine and PGs, give atropine and steroids, ttt of the cause e.g. PRP
Chronic uveitis leads to 2ry glaucoma by :
PAS, or occlusion pupillae, seclusion pupillae
In hypermature cataract , deep AC, severe pain, corneal edema
Lens protiens leak through intact capsule
Deposition of dandruff like basement meemb. Like material on lens and angle ,
Weak zonule: risk of sublax.
Ttt as POAG
