Glaucoma
D E FI N I T ION
Optic neuropathy with typical field defect usually associated with ocular
hypertension (intra-ocular pressure, IOP > 21 mmHg).
AE T IOLOGY
Primary causes:
Acute closed-angle glaucoma (ACAG), primary opened-angle glaucoma
(POAG), chronic closed-angle glaucoma.
Secondary causes:
Trauma, uveitis, steroids, rubeosis iridis (diabetes, central retinal vein
occlusion).
Congenital:
Buphthalmos, other inherited ocular disorders.
E P IDEMIOLOGY
Prevalence 1 % in over 40 years, 10 % in over 80 years (POAG).
Third most common cause of blindness worldwide.
H ISTORY
ACAG:
Painful red eye, vomiting, impaired vision, haloes around lights.
POAG
: Usually asymptomatic, peripheral visual field loss may be noticed.
Congenital: Buphthalmos (ox eye), watering, cloudy cornea.
EXAMINATI ON (BY S L I T-LAMP)
ACAG: Red eye, hazy cornea, loss of red reflex, fixed and dilated pupil, eye tender and hard on
palpation, cupped optic disc, visual field defect (arcuate scotoma), moderately raised IOP.
POAG: Optic disc may be cupped. Usually no signs.
PATHOLOGY/PATHOGENESI
S Ocular hypertension compresses and stretches the retinal
nerve fibres leaving the optic disc causing scotomas and visual field loss. Ocular
hypertension is caused by # outflow of aqueous humour caused by:
. obstruction to outflow by approximation of iris to cornea closing iridocorneal angle and
trabecular meshwork/canal of Schlemm causing a rapid and severe rise in IOP (ACAG);
. resistance to outflow through trabecular meshwork (POAG); or
. blockage of trabecular meshwork by blood or inflammatory cells.
INVE S T I G A T IONS
Goldmann Applanation Tonometry: Standard examination to measure ocular pressure
(normal 15 mmHg, POAG 22–40 mmHg, ACAG> 60 mmHg).
Pachymetry: Using ultrasound or optical scanning to measure central corneal thickness
(CCT). CCT <590mm are at higher risk of developing glaucoma.
Fundoscopy: To detect pathologically cupped optic disc (cup – disc ratio > 0.6 or an
asymmetry of 0.2). Picture record of optic nerve head is recommended.
Gonioscopy: To assess the iridocorneal angle.
Perimetry (Visual field testing): For arcuate scotoma (early), tunnel vision (late).
MANAGEMENT1
ACAG (medical emergency): IV acetazolamide (500 mg), 4% pilocarpine topically, analgesics,
antiemetics. May require emergency iridotomy.
Long-term (topical hypotensives)2
b-blockers (timolol): # Aqueous humour secretion.
Prostaglandin analogues (Latanoprost): " Flow via uveoscleral drainage.
Carbonic-anhydrase inhibitor (dorzolamide): # Aqueous humour secretion.
Parasympathomimetics: Pilocarpine (constricts pupil, opening up the trabecular meshwork).
Sympathomimetics: Brimonidine (a2-agonist).
1NICE 2009 guidelines are available on the management of glaucoma at: http://www.nice.org.uk.
2The Ocular Hypertension Treatment Study (OHTS) showed that topical hypotensives prevent or delay the
development of glaucoma.
Glaucoma (continued)
Surgery:
Laser treatment: Laser trabeculoplasty for POAG; iridotomy for ACAG.
Conventional: Trabeculectomy, canaloplasty or iridectomy facilitates outflow of aqueous
humour. 5-fluorouracil or mitomycin may be used to reduce scarring.
COMPL I C A T IONS
Congenital: Amblyopia and visual loss.
POAG: Visual loss.
ACAG: Visual loss and anterior synechiae.
P ROGNOS I S
Poor prognosis for congenital glaucoma caused by amblyopia. Prognosis in
acquired glaucoma depends on early diagnosis and treatment.
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