6.1.8. Evaluates glaucoma risk factors to detect glaucoma and refer accordingly.

Question 1

Glaucoma Risk Factors

Answer 1

• IOP – higher pressure = more likely & disease is usually more aggressive/rapid
  o Asymmetry of 4mmHg or more is significant
• Age – older >40
• Family history – 6-fold increase if 1st degree relative

Question 2

POAG, risks

Answer 2

• Race – 4x more common in individuals of African descent
• Myopia >4D
• Large optic disc
• Thin cornea
• Diabetes
• High blood pressure
• Peripheral vascular disease
• Contraceptive pill
• Ocular hypertension – 10% over 5 years / asymmetry >4mmHg

Question 3

NTG risks

Answer 3

• Ethnicity – Japanese 4-12x more likely
• Myopia >4D
• Raynaud’s Phenomenon
• Migraine
• CCT tends to be lower than in POAG
• Gender – females
• Systemic hypotension
• Myopia
• Thyroid disease

Question 4

PACG

Answer 4

• Race – far eastern and Indian Asians
• Refraction – hypermetropic
• Short axial length – narrow AC
• Age >40 – AC becomes narrow as lens becomes thicker
• Gender – females
• Family history – genetic factors are important but poorly defined
  *

Question 5

Secondary glaucoma’s

Answer 5

Pseudoexfoliation (open angle)
* PXF = grey-white fibrillary amyloid-material
* Symptoms worsen following exercise

Pigment dispersion (open angle)
* Young, white, myopic males
* Pigment is deposited on corneal endothelium Krukenberg spindle

Hyphaemia (open angle)
* Blood in AC caused by trauma

Phacomorphic (closed angle)
* Lens size increases and blocks drainage

Rubeosis iridis may lead to neovascular glaucoma
* Pxs with ischaemic CRVO / DR are at risk of developing this
* Iris forms membrane onto TM and new vessels grow within the angle

Question 6

Primary open angle glaucoma

Answer 6

• Open drainage angle
• Occurs in the absence of any other ocular, systemic or pharmacological cause and accompanied by IOP >21mmHg
• 2 proposed mechanisms by which raised IOP is thought to cause glaucomatous damage
• Vascular dysfunction - results in ischaemia to optic nerve
• Mechanical dysfunction/ trabecular dysfunction - trabecular meshwork gradually becomes less effective allowing aqueous to pass through to Schlemm’s canal (increased outflow resistance)

Question 7

Normal tension glaucoma

Answer 7

• Glaucoma without evident secondary cause which follows a chronic time course and occurs in the presence of an open anterior chamber angle
• OAG where IOP has rarely been recorded above 21mmHg
  Proposed mechanisms:
  1. Higher sensitivity to normal pressure
  1. Vascular dysregulation
  1. Abnormally high translaminar pressure gradient
  1. A neurodegenerative process due to impaired cerebrospinal fluid dynamics in the optic nerve sheath compartment

Question 8

Angle closure glaucoma

Answer 8

• Group of conditions that result in closure of the anterior chamber angle, ultimately resulting in glaucoma
• Different mechanisms which can cause angle closure
  1. Pupil block - failure of aqueous flow through pupil leads to a pressure difference between anterior and posterior chambers, resulting in anterior bowing of the iris
  1. Non-pupillary block - important in many far eastern patients, associated with a deeper AC than pure pupil block

Question 9

Chronic angle closure

Answer 9

• The iris slowly comes into contact with an increasing area of trabecular meshwork, resulting in TM dysfunction and a gradual rise in IOP
• • Gradual and/or spiking of IOP causing optic disc damage that looks like that of OAG
• Open but narrow angle or shallow AC / ITC on gonioscopy – irido trabecular contact – if the iris touches the trabecular meshwork
• Hypermetropia – above 2/3D

Question 10

Intermittent angle closure

Answer 10

• The angle is narrow but open, but certain physiological states (producing dilation) lead to transient rises in IOP which resolve over variable periods of time
• This often produces transient symptoms of acute angle closure
• Intermittent brow ache, haloes
  *

Question 11

Acute angle closure and sx

Answer 11

• Dilation of pupil leads to angle closure
• Marked rise in IOP due to: pupil block (pupil builds up behind iris and pushes it forwards) or peripheral iris tissue occluding the angle - often present at the same time.
• Blurred vision/haloes
• Brow ache/headache
• Nausea
• Red eye
• Fixed mid-dilated pupil
• Hazy blue/green cornea – caused by the way the light is reflected/refractive when the cornea is oedematous
• Iritis
• IOP > 40mmHg
• Shallow AC

Question 12

Glaucomatous disc features

Answer 12

1. C:D ratio
2. Blood vessel position
3. Rim thickness
4. Pallor
5. Peri-papillary atrophy
6. APON (acquired pit of ON)
7. Haemorrhage
8. Nerve fibre layer defects
9. Notches – like APONs, highly focal loss of tissue
10. Laminar dots
11. Nasalisation of BVs

Question 13

Cup to disc ratio relevance depends on

Answer 13

• Since the ONH has a direct bearing on degree of cupping, it is essential to estimate the overall disc diameter
• The best method to do so is using the beam of a slit lamp
• Multiplication factors
• 60D – 1.0
• 78D – 1.1
• 90D – 1.4
• Superfield – 1.5
• Small disc – less than 1.5mm
• Medium disc – 1.5-2.0mm
• Large disc - greater than 2.00
• Important to measure vertically
• Superior and inferior aspects contain the most neural tissue and therefore are where changes are most likely to be identified first
• Interpret results alongside disc size
• NICE indicate that a 0.2 difference is clinically significant
  *

Question 14

Assess width of NRR

Answer 14

• Narrowest rim/disc ratio should be recorded & considered alongside additional indicators of glaucoma
• In general, ON is positioned slightly superiorly to the horizontal raphe, as a result the inferior aspect has the greatest concentration of ganglion cell axons
• In most discs, this translates that inferior is where the NRR is broadest
• (DDLs)
  *

Question 15

PPA

Answer 15

• More prevalent in areas with NRR damage
• Alpha zone PPA (black arrows) = areas of increasing irregular RPE pigmentation. This is supposed to occur first, and as there is an increasing RPE loss, so it develops into beta zone PPA
• Beta zone PPA (blue arrows) = areas of partial or complete loss of RPE and some choriocapillaris, with visibility of larger choroidal vessels becoming more apparent
• It is found adjacent to the ONH

Question 16

Focal NRR loss

Answer 16

• Occurs in a localised area of tissue, usually at the poles of the disc
• More common in NTG
  *

Question 17

Diffuse NRR loss

Answer 17

 Occurs when ganglion cells are lost in a more uniform manor
 More common in POAG

Question 18

Disc haemorrhages

Answer 18

 Often first sign of a problem
 All/some of haemorrhage contained within optic disc
 More common in NTG
 Blood cells in the superficial layers of the ONH will be flame/feather shaped
 More subtle haemorrhages occur when blood is released into deeper layers before axons go through the 90-degree bend; appear as faint dot haemorrhages

Question 19

Bayonetting of blood vessels

Answer 19

 When thinning of the NRR reaches the disc margin, a sharpened rim is produced
 If a retinal vessel crossing sharped rim, it will bend sharply at the end of the disc

Question 20

Baring blood vessels

Answer 20

 i.e., flyover vessels
 baring occurs with enlargement of the cup
 The rim narrows and leaves the vessels isolated/bared

Question 21

Laminar dots/changes in laminar cribrosa

Answer 21

 Laminar cribosa becomes more visible
 Pores in laminar cribrosa become more visible, enlargement of pores indicate RNFL loss

Question 22

Disc pallor

Answer 22

 Disc pallor is more likely to be another optic neuropathy
 Ensure you check for: altitudinal VF defect / RAPD

Question 23

RNFL loss

Answer 23

 RNFL defects represent the drop out of anterior bundle of ganglion cell axons
 Nerve fibre bundle defects are often the repeat of repeated disc haemorrhages
 They are best seen with red-free light and clear media, and appear as dark wedge shape originating from the disc margin against the lighter striations of the NFL
 For large defects, localised notching of the NRR is often seen where the defect meets the disc margin

Question 24

IOP

Answer 24

 Mean 15.5 mmHg
 Standard deviation 2.5mmHg
 Normal range 10-21mmHg
 IOP should be similar between eyes
 Approx. 33% of glaucoma patient have NTG with IOP <21mmHg
 Majority of eyes with IOP over 21mmHg = no detectable signs of glaucoma = OHT

 Higher mean IOP in black ethnicity (18.7mmHg)
o Also have thinner corneas; potential for tonometry errors and decreased tolerance to raised IOP
 Lower mean in people of Asian ethnicity; especially east Asian (13mmHg)
 Family history
o Higher IOP with FHx of OHT or glaucoma

Question 25

Pachymetry & CCT

Answer 25

 Pachymetry = measurement of CCT
 Normal = 555 microns
 Range 480 to 600 microns
 Corneal thickness = thicker in periphery
 Variations
o Diurnal = thicker in the morning (oedema)
o Disease = thicker in Fuch’s
o Age = CCT decreased with age in Asian people
o Ethnicity = black people have corneas that are 17-60microns thinner than white
 Thinner cornea = less force to applanate = under estimation
 Thicker cornea = more force to applanate = over estimation
 Eyes with thinner corneas have:
o 3 times increase risk of glaucoma
o Earlier VF loss and more advanced disease at diagnosis

Question 26

Other corneal properties which affect IOP

Answer 26

 Corneal oedema = after CL wear / sleep = overestimation of IOP
 Biomechical effects e.g., corneal rigidity = may affected IOP as much as CCT
 Corneal curvature
o Steep = overestimation
o Flat = under estimation

Question 27

Visual fields

Answer 27

**Paracentral **

 Usually in the superior VF initially; may be relative or absolute
 Scotoma may be single or multiple and can increase in number / join to form arcuate defects
 Paracentral defects are thought to occur more commonly in cases of low / NTG

**Arcuate **

 Due to localised partial or complete damage to a nerve fibre layer bundle and scotoma follows the shape of this bundle
 Gives rise to characteristic defect, which can be absolute, relative or combination of both
 As the disease progresses, these arcuate defects may extend in an arcuate shape from the upper and lower poles of the blood spot
 They can then widen into the peripherally and centrally, eventually leaving the patient with only a central island of vision

Nasal step

 Nasal step describes the most remote end of an arcuate defect
 Vertical discontinuity across the raphe in the temporal retina gives sharply delineated step in the nasal field plot when comparing superior and inferior hemifields

**Combination **

 VF defects can also occur in combination e.g., nasal step and an arcuate defect

Overall depression

 An overall depression can also be a soft sign of glaucoma caused by global RNFL damage
 There are many other causes for an overall depression; therefore it is only a soft sign

**Enlargement of blind spot **

 Soft sign, results from NFL defects at the disc

Question 28

Glaucoma (SIGN GUIDELINES) for routine referral

Answer 28

 Optic disc signs consistent with glaucoma
 Reproduceable VF defect in either eye
 Risk of angle closure (VG G1 / gonio > 270deg TM not visible)
 OHT IOP >25mmHg, irrespective of CCT
 OHT - IOP <26mmHg and CCT <555
o OHT meaning IOP >21mmHg
 Emergency / same day for IOP >40mmHg / red eye / angle closure

Target IOP – IOP that is expected to confer optic nerve stability in px with glaucoma based on glaucoma damage, life expectancy, untreated IOP reading, additional risk factors & rate of progression

Question 29

Topical hypotensive

Answer 29

1. Prostaglandin analogue e.g. Latanoprost (Xalatan)
    Increase uveoscleral outflow by ciliary muscle relaxation
    30-35% IOP reduction
    Main ADRs: iris hyperpigmentation & eyelash changes
2. Beta-blocker e.g. timolol,
    Decrease aqueous production
    25-30% IOP reduction
    Increase risk of systemic side effects e.g. systemic hypotension, exacerbation of asthma, heart failure
   o Do not give to asthmatics/COPD/heart issues
   o Do not give px already on beta-blocker for hbp; this will already have a IOP lowering effect, if still high then topical beta-blocker may not have much of an effect as it works in the same mechanism
3. Carbonic anhydrase inhibitor e.g. brizonolamide (azopt)
    Decrease aqueous production
    18% IOP reduction
4. Alpha 2 agonist e.g. brimonidine tartrate (alphagan)
    Decrease production & increase outflow
    25% IOP reduction