Pre-Reg Stage 1 Visit 1 - Glaucoma

What are RF for POAG?

• Age - increases significantly with age - 80 y/o is 4x more at risk than 50 y/o

• Ethnicity - African/Caribbean + Latino px from Mexico, Brazil, Argentina - diff in connective tissue stiffness

• FMH - increased risk by 2-4x - 2.17x if parent, 3.69x if sibling 

• Males - 1.37x more likely 

• Myopes - 2x more risk than emmetropes - BUT increased risk with higher Rx e.g greater than -6.0D

• Raised IOP - although 50% of POAG px have IOP within normal range

• DM  - can lead to neo glaucoma + a substance known as fibronectin can obstruct drainage

What is the most powerful modifiable RF for POAG?

• Raised IOP

• Lowering the IOP significantly reduces the risk of POAG - common using prostaglandin analogues

• e.g lowering IOP by 20% approx. halved the risk of POAG

Systemic conditions that are RF for POAG

• Raynaud’s Phenomenon - vascular circulation is compromised at fingers/toes 

• Diabetes, systemic hypertension, migraine, sleep apnoea - all increase risk but considerably less than other RF

What is IOP elevation caused by, in Glaucoma and how does this link to POAG?

• Restricted drainage rather than overproduction by the ciliary body

• POAG occurs without any visible obstruction to outflow (e.g closed angle) however drainage is nevertheless compromised

where are the apertures larger and where is greater atrophy seen?

• Larger apertures in the superior and inferior regions and smaller across the horizontal 

• Greater atrophy is seen in the larger lamina cribrosa aperture regions - VERTICAL - less support

How does Elevated IOP cause damage to RGCs?

• Elevated IOP induces biomechanical deformation of the Lamina Cribrosa - it bows posteriorly placing mechanical strain on the RGC axons passing through it 

• This deformation also limits the ability of RGC axons to transport Brain-Derived Neurotrophic Factors from the LGN to RGC cell body

• BDNF - critical to RGC health - lead to cell death if absent 

• RGC cell bodies can also be directly compromised and VF defects can occur anywhere across the retina

What regions are more prone to IOP-induced stress?

• Inferior and superior temporal retina due to less support for LC apertures in the vertical meridian + RNFL thinnest @ T

• As a result VF loss often begins in the superior and inferior nasal regions

What are the primary structural changes in Glaucoma?

• Bowing of the LC posteriorly

• Loss of RNF tissue - pre-laminar unlike AION

Signs of structural changes of the ONH?

• Thinning of the RNFL - ISNT rule? If previously followed ISNT rule but doesn’t now - suspicious 

• Thinning of NRR - Pale NRR - irregularity in pallor around the NRR can be a sign of glaucomatous damage

• Excavation of the ONH = increased cup depth - occurs due to RGC atrophy = loss of RNFL 

• Increased CD ratio - increasing proportion of the disc takes the colour of the cup

Other uncommon Signs we may see in POAG

• Bayonetting of retinal vessels - sign of RNF atrophy

  • Where retinal vessel disappears as it descends the slot of the cup wall before reappearing

  • Bends up to 90 degrees when it descends into the cup 

• Acquired Optic Disc pit; focal depression within the cup - usually inferior

Why does NRR look pale / increased pallor?

• Arises due to increased light reflectance caused by nerve fibre atrophy - less light is absorbed by the thinned RNFL 

• More light being reflected back to us from the LC

What does the sign splinter haemorrhages tell us?

• Px is ongoing glaucomatous disease progression rather than a RF of potential ONH damage

What are the common VF defects seen in Glaucoma?

• Paracentral defects - LEFT

• Arcuate VF defects - commonly in the superior and inferior NASAL regions - correspond with RGC death at Inferior and Superior temporal retina - RIGHT

• If defects become more dense then referred to as altitudinal defects

Both defects don’t cross the horizontal midline

At what point will these VF defects cause Sx and the importance of VF?

• If they are very close to fixation (macula) - uncommon in glaucoma

• VF defects in both eyes overlap to induce a defect that is visible binocularly

• VF defects will only be picked up on machines at the later stage of glaucoma atp where there may be irreversible VF loss

• It is important to not rely on just VF results to base on whether the px has glaucoma or not

When would you refer for suspected POAG / OHT?

Refer if;

• ONH damage consistent with glaucoma in either eye - any acquired optic pathology requires ophthalmological opinion regarding possibility of progressive ONH damage - can refer just off this

• If IOP in either eye is equal to or greater than 24mmHg even if this is the only finding - measured by GAT

• VF defect consistent with glaucoma detected in either eye - refer even if only abnormality 

• A narrow angle on van Herick with risk of angle closure 

• Conditions that can cause secondary glaucoma e.g pseudoexfoliation / PDS

What would the urgency be on suspected POAG and what are the exceptions?

• Routine 

Except in the case where there is a risk of angle closure or if pressure is greater than 35mmHg and there is VF loss

What should an Optometrist do in the case of 24mmHg or higher measurement via NCT?

• Remeasure IOP using GAT - OPTOM needs to be accredited to perform ‘supplementary’ tests

• Allows reimbursement via an additional fee paid by the ICBs - shared care schemes / referral refinement

• Shared care schemes aim to reduce false positive

If a px has 24mmHg via NCT and there is no shared care scheme what should you do?

• If there isn’t any additional reimbursement from shared care schemes then no requirement to do GAT

• Refer based on the NCT alone, regardless of how it was measured

• If referring off NCT - Take at least FOUR readings per eye and use the MEAN as the result

• Ensure to note on the referral letter that it was done by NCT - HES will complete GAT

When should IOP and VF routinely be done?

• Px with ethnic risk of Glaucoma

• Over the age of 40

• FH of Glaucoma

• Px taking topical or systemic steroids - could develop steroid induced glaucoma

What is an Ocular Hypertension Monitoring Service?

• For px who have been through Glaucoma assessment at HES 

• For those who have persistent elevated IOP but no Glaucomatous ONH damage / VF loss 

• If high street Optom has been accredited then can monitor Px in practice in a specific OHTMS appt

What is the inclusion criteria for OHTMS?

• Px diagnosed with OHT but don’t require treatment - e.g IOP lower than 24 can still be OHT but won’t receive treatment

• Px diagnosed with OHT who are on IOP lowering drugs and they’re currently at their target IOP

• Pseudoexfoliation Syndrome or PDS with IOP >24mmHg but no other signs of Glaucoma

What is the criteria for referral back to HES Glaucoma clinic? (When Optom is accredited to monitor px in practice via OHTMS)

• IOP > 32mmHg - assess using GAT

• IOP > target IOP - assess using GAT

• Signs of progressive Glaucomatous ONH damage / VF defect

• If there is a clinical need to repeat gonioscopy, repeat CCT measurement

• Side effects or poor compliance to medication

• Any other changes requiring specialist opinion

Medical Management of POAG

• Eyedrops are the initial treatment plan for majority of Px

• Common goal of reducing IOP - seen as an indirect way to control glaucoma

• Before initialising treatment there will be a Target IOP set by the Ophthalmologist - usually 30-50% lower than baseline IOP

What drops are the first line treatment for POAG?

• Prostaglandin Analogues OR BB - both reduce IOP by around 20-35%

• PA are more commonly prescribed due to being highly effective and are safe to use - rare produce serious ADR

• BB carry the risk of reductions in HR and constriction of the airways + bronchial system

How do Prostaglandin Analogues work?

• Increase outflow of AH via Uveal-scleral pathway

• Used Once a day, preferably in the evening

• - prost ending e.g latanoprost, travoprost, bimatoprost

What are the ADRs to PA?

• Local irritation, stinging and hyperaemia 

• 25% of px report iris darkening within 6 months

• Thickening and lengthening of eyelashes - cosmetic without any health implications

• Rarely these drugs can lead to CMO, recurrence of Anterior uveitis or HSV - all merit urgent referral

How do Beta-Blockers work?

• Inhibit the production of AH

• Use 2x daily 

• -olol ending e.g timolol, levobunolol, betaxolol

What are the ADRs to BB?

• Dry eyes commonly reported + Ocular irritation & redness

• Slow the HR - contraindicated in Px with Bradycardia (when resting HR is less than 60 bpm)

• Promote constriction of the airways - contraindicated in Px with asthma or Obtrusive airway disease

What is second line treatment for POAG?

Xalacom - contains both PA & BB - latanoprost + timolol

What drugs are used in third line treatment of POAG?

• Alpha-2 Agonists 

• CAI

Alpha-2 Agonists

• Inhibit the production of AH and increase outflow via uveal-scleral pathway

• Used 2x daily

• -dine ending e.g brimonidine, aprachlonidine

• ADR - ocular allergy, dry mouth, fatigue and drowsiness

• AVOIDED IN PX USING MONOAMINE OXIDASE INHIBITORS - treatment for depression

Carbonic Anhydrase Inhibitors

• Inhibit the production of AH

• Used 2/3x daily

• -zolamide ending - e.g dorzolamide

• Alternative/combination with BB

• ADR - Irritation and redness of instillation, bitter taste & dry mouth, allergic conjunctivitis

What drugs suggest POAG is advanced?

• If Px is using BB (timolol) in combination with a CAI (dorzolamide) 

When would a Px be recommended for surgery to treat POAG?

• If px doesn’t respond to IOP lowering drugs

• Drugs produce ADRs 

• Poor compliance

• Advanced Glaucomatous damage - need to preserve vision so require rapid drop in IOP

What surgical management is available for POAG?

• Selective Laser Trabeculoplasty (SLT)

• Guidelines from 2022; SLT should be offered as first line treatment in

• Px with OHT and IOP greater than 24 if they are at risk of VI within their lifetime

• Px who are newly diagnosed POAG - recent evidence suggests this is more effective then IOP lowering drops

How does SLT work?

Using a laser to create burns in the TM which improves outflow of AH

What are the RF for NTG?

• AGE - tend to be older than POAG

• +FH

• East Asians (Japanese)

• Low CCT

• Abnormal vasoregulation (migraines, Raynaud’s)

What is NTG

• Pressures lower than 21mmHg with Glaucoma damage/VF defect - same Tx as POAG

What are the RF for PACG?

• Risk increases sharply with age - especially when 70 and above - due to growth of lens which extends to AC and increases risk of Pupil Block

• +VE FH - 3-4x more likely 

• Asian ethnic background

• Hypermetropes - shorter axial lengths and shallower AC than myopes 

• Females - 3x more likely

• MEDS - Topiramate/Sulfonamides

Why does PACG occur?

• Occlusion of the anterior chamber angle - specifically occlusion of the TM by Peripheral Iris - making contact with the posterior cornea

• TM is the main route of drainage of AH - obstruction causes volume of AH to increase in the AC = rise in IOP

What is Acute PACG and what are its Sx?

• Angle closure develops suddenly leading to a sudden spike in IOP

• Sx include severe pain and blurred vision - suddenly reduce to 6/60 or worse

• Halos around light - due to oedema in the corneal stroma

• Headaches 

• Nausea + Vomiting 

• Red eye

• Acute form is usually intermittent - SX are also intermittent

What is chronic PACG?

• Longstanding, partial closure

• Mild sx, many asymptomatic 

• IOP (likely to be <40mmHg) is sufficient to cause Glaucomatous ONH damage

What is the pathway of AH?

Flow of aqueous from the posterior chamber (where it is produced), through the pupil, to the anterior chamber - where it is drained through the TM

What does the Pupil Block cause and where is it blocked?

• Prevents AH flowing from the posterior chamber to the anterior chamber

• The block occurs as the posterior iris attaches to the anterior surface of the lens - block created a

Why is an Iris Bombe caused and what is the consequence of it?

• Caused by the increase in pressure within PC, pushes on the posterior surface of the iris causing the iris to bow forward

• Due to this the peripheral iris is brought into contact with the posterior cornea - termed irido-trabecular contact

What occurs if irido-trabecular contact is persistent?

• Peripheral anterior synechiae 

• Blocks the anterior chamber angle + TM  via Canal of Schlemm, preventing any drainage of AH from the AC

What are the potential causes of angle closure via pupil block?

• Due to shorter axial length - hyperopes

• Shallow AC 

• Can occur due to pharmacological dilation - increased risk of peripheral iris becoming attached to lens

What are the signs of Acute ACG?

• Raised IOP >40mmHg - could be as high as 80mmHg

• Pupil relatively fixed and sluggish response to light

• Pupil will appear vertically-oval and semi-dilated 

• Corneal Oedema - cornea will appear cloudy

• Cells & Flare in AC

• ONH damage is unlikely in Acute form as ONH changes are associated with chronic IOP elevation over months/years

• Dilated scleral/episcleral BV

What are the signs of Chronic PACG?

• Glaucomatous ONH damage

• Potentially VF defect 

• Chronic raised IOP - around 40mmHg or less

• VH will show angle grade 2 or below

What is the difference between POAG and chronic PACG?

• In PACG there is a physical obstruction causing the IOP elevation (irido-trabecular contact)

• POAG there is no obvious physical cause of the IOP elevation

What is the Optometric Management of Acute PACG?

• Emergency Referral - same day

• Phone local HES to explain findings

What is the Optometric management of Chronic PACG?

Routine referral

What is the Ophthalmological management of Acute PACG?

• Initially use MEDS to control IOP;

  • Osmotic agents 

  • Acetazolamide (CAI)

  • Pilocarpine

  • Prostaglandin Analogues

  • Topical Beta-Blockers

Main treatment is Peripheral laser iridotomy

What examples are there of Osmotic Agents?

• Glycerol - ORAL

• Isosorbide - ORAL

• Mannitol - intravenously

How does Pilocarpine reduce IOP?

Miotic drug that encourages constriction of the pupil - aims to break the pupil block

How does Peripheral Laser Iridotomy work?

• Laser in the peripheral iris tissue creating a hole

• This acts as an extra channel for AH to drain from the post. chamber to the ant. Chamber

• Used to treat current case but also prevent future acute attacks

• It will often be performed in the other eye as a preventative measure

What is being seen as a more effective treatment than iridotomy?

Crystalline lens extraction - using a thinner IOL = open angle

What is Pseudoexfoliation Syndrome?

• Build up of white, flaky, dandruff like material which clogs up the TM - impedes outflow of AH - rise in IOP

• Usually unilateral but affects BE over time

• One of the most common causes of Secondary Glaucoma

What are the RFs for pseudoexfoliation syndrome?

• Prevalence increases with age - rare in younger than 50s - 6.25% in Adults ages 85 and older

• Women at more risk

• Scandinavian countries + Greece

What are the Signs of Pseudoexfoliation syndrome?

• Material can be viewed on the lens and pupil margin 

• ‘Bullseye’ pattern on the lens - central disc and outer ring of pseudoexfoliative material separated by a clear band - RARR

• Central disc of material - white, granular appearance

• Pupil dilation is indicated to ensure that any peripheral pseudoexfoliative material can be viewed

• BARR - tufts of PE material

• BLUARR - PE material that wouldn’t be seen s Dilation

Management of Pseudoexfoliation syndrome?

Routine referral - irrespective of signs of glaucoma

What is Pigment Dispersion Syndrome (PDS)?

• Release of Pigment granules from the Iris pigment epithelium which lines the back surface of the iris

• Carried by the currents of AH flow through the AC to reach the TM

• Deposition of these granules leads to clogging up of the TM and rise in IOP - same as PES

• Second most common type of secondary Glaucoma

How may PDS arise?

• Release of Pigment granules is typically gradual = Chronic rise in IOP

• In some cases a rapid release can cause a Spike in IOP 

• Acute Phase of PDS is precipitated by undertaking physical exertion e.g exercise

What are the RFs for PDS?

• Males

• Caucasian

• Myopia 

• More common in younger Px - 20 to 50 y/o

What are the signs of PDS?

• Radial - transillumination defects - particularly in blue irides

• Pigment granules will be deposited on the posterior cornea (corneal endothelium)

How do the pigment granules on the posterior cornea appear?

• As a thin, vertical line - referred to as a Krukenberg Spindle

• Brown-gold iris pigment is visible 

• This shape is caused by the direction of the AH currents which flow through the AC

Why do steroids cause a rise in IOP?

• Leads to reduced aqueous outflow via TM

What should all Px taking corticosteroids do?

• Should have their IOPs monitored on a monthly basis

• This should happen at the hospital that prescribed the steroids

What is the treatment for Secondary CAG?

• Use of a mydriatic drug - breaks the adhesion between posterior iris and anterior lens - post synechiae

• This stops AC angle closing due to iris bombe