Glaucoma

Question 1

def glaucoma

Answer 1

Optic neuropathy with typical field defect usually associated with ocular hypertension (intra-ocular pressure, IOP>21 mmHg).

acute closed angle glaucoma - angle of anterior chamber narrows acutely - sudden rise in IOP to >30mmHg, pupil becomes fixed and dilated and axonal death(retinal ganglion cells) occurs.

IOP may be raised, but this is not part of the definition.

Question 2

primary causes glaucoma

Answer 2

Acute closed-angle glaucoma (ACAG),

• primary angle closure - pts have predisposition anatomically
• secondary angle closure - from pathological processes (eg traumatic haemorrhage pushing the posterior chamber forwards).
• RF - increased age and hypermetropia

primary opened-angle glaucoma(POAG),

chronic closed-angle glaucoma.

Question 3

secondary causes glaucoma

Answer 3

Trauma,

uveitis,

steroids,

rubeosis iridis (diabetes, central retinal vein occlusion).

Question 4

congenital causes glaucoma

Answer 4

Buphthalmos,

other inherited ocular disorders

Question 5

chronic simple (open-angle) glaucoma RF

Answer 5

raised IOP

black race

FH

older

HTN and dm

Question 6

path glaucoma

Answer 6

Ocular hypertension compresses and stretches the ret-inal nerve fibres leaving the optic disc causing scotomas and visual field loss.

ocular HTN caused by reduced outflow of aqueous humour because

• obstruction by approximation of iris to cornea closing iridocorneal angle and trabecular meshwork/canal of Schlemm = rapid and severe rise in IOP (ACAG)
• resistance to outflow through trabecular meshwork (POAG)
• blockage of trabecular meshwork by blood/inflamm cell

Question 7

epi glaucoma

Answer 7

Prevalence 1 % in over 40 years, 10 % in over 80 years (POAG).

Third most common cause of blindness worldwide.

ACAG - 40-60yrs, more common in Asia

~10% of blind registrations in the UK are attributed to glaucoma. It aff ects ~2% of the population >40 years old.

Question 8

sx glaucoma

Answer 8

ACAG: Painful red eye, vomiting, impaired vision, haloes around lights, headaches, uniocular attacks. Onset is over a few hrs/days

POAG: Usually asymptomatic, peripheral visual field loss may be noticed.

Congenital: Buphthalmos (ox eye), watering, cloudy cornea

chronic simple (open-angle) glaucoma

• asymptomatic until visual fields are badly impaired - need screening
• Visual field loss may manifest as dangerous difficulty dodging cars while crossing busy roads.

Question 9

signs ACAG

Answer 9

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.

Question 10

signs POAG

Answer 10

Optic disc may be cupped. Usually no signs.

Question 11

signs glaucoma

Answer 11

on field testing, 3 or more locations are outside normal limits, and the cup-to-disc ratio is greater than that seen in 97.5% of the population

IOP >21mmHg may or may not correlate with cupping, nerve damage, with scotomata (sausage-shaped fi eld defects near the blind spot, which may coa-lesce to form big defects).

ince the central fi eld is intact, good acuity is main-tained, so presentation is often delayed until irreversible optic nerve damage.

The visual defects tend to be bilateral, although are not always symmetrical. Some get glaucoma with normal IOP (eg if retrobulbar blood flow reduced)

Question 12

ix glaucoma

Answer 12

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 anasymmetry of 0.2). Picture record of optic nerve head is recommended.

Gonioscopy: To assess the iridocorneal angle, Peripheral anterior chamber configuration and depth assessments

Perimetry (Visual field testing):For arcuate scotoma (early), tunnel vision (late).