Glaucoma Care by Optoms in Bristol

This was another really good lecture! There was a HUGE amount of info in it that I can't hope to replicate here. Go back to the actual notes and read read read.

It's probably good to summarise glaucoma again. Hammer it in like. It's a variety of diseases with a common denominator - ACQUIRED PROGRESSIVE OPTIC NEUROPATHY. If it's untreated/unsufficiently treated it will lead to progressive loss of visual function. There are a variety of different causes and so a variety of different types/diagnoses. Let's categorise::::

• Open-Angle without ocular or systemic disorders - POAG, Normal Tension Glaucoma
• Angle closure without known ocular/systemic disorders - pupillary block glaucoma, combined mechanism glaucoma
• Developmental glaucomas - congenital, glaucomas assoc w/oc/systemic anomalies, 2ary glaucomas in childhood
• Glaucomas assoc w/oc/sys disorders - assoc w/disorders of endothelium, iris & cil body (pigmentary), lens, retina/choroid/vitreous, assoc w/intraocular tumours, elevated episcleral venous pressure, inflammation, steroid induced glaucoma, ocular trauma, haemorrhage, following intraoc surgery

Chronic Open Angle Glaucoma - Glau w/out ocular/systemic associations

• Epidemiology - onset from 35yr onwards, prevalence 2% (relatively common)
• Risk Factors - major ones are IOP and age, moderates are race and family history, minor are vasculopathy, vasospasm and lot central corneal thickness
• Subdivs - high pressure type (POAG), normal pressure type (Normal Tension Glau)
• Definition - multifactorial glaucoma w/characteristic progressive atrophy of ON head (not exactly sure of cause)
• Cause(s) - mechanical, vascular, autoimmune?
• Heredity - mostly unknown, few genes identified
• IOP Elevation - variety of angle degenerative changes
• Symptoms - none til advanced
• Signs - Physiological open angle, acquired disc/RNFL signs, VF signs
• Course - usually slowly progressive
• Visual prognosis is good cf age, how bad it is when first detected

Why should optoms take a greater involvement in glaucoma care?

• Causes blindness & visual morbidity
• Has substantial impact on the current NHS HES resources
• Optoms are already part of the pathway doing 95% of the glaucoma related referrals
• They have many of the tools/skills to equip them for an extended role
• The new prescribing legislation for optoms can be applied to glaucoma management
• College Glaucoma Higher Qualifications have been established
• NICE Glaucoma guidance is on the way
• The DoH trials of alternative glaucoma pathways have recently been completed
• International critical mass of glaucoma specialist optometrists

In 2004 'supplementary prescribers' were defined and in 2009 'independent prescribers'. Sup. prescribing extends the role of the prescriber to make better use of their knowledge and skills and is suitable for optometric co-management.

The Upcoming Clinical Challenge

Glaucoma is currently the second most common cause of CVI certifications. It has a better prognosis if treated in the disease's earlier stages. Early glaucoma is hard to identify. It's a chronic condition that requires lifelong review and is dominated by medical treatment. Obviously there is a public health issue as a significant proportion of cases may remain undetected.

The population of the UK is growing and ageing. There is expected to be a 12% growth in numbers and 8% shift towards the higher glaucoma prevalence age bracket (over 65 years). Life expectancy is also increasing (2002 women age 84, 2020 88) which obviously means more people having their glaucoma review. In summary, more people will be requiring more appointments for a longer period. Maths suggests that there'll be an extra 390,000 appts required per year by 2031 and current increases in ophthalmologist training are unlikely to meet this demand.

The Bristol Shared Care Scheme

Included peoples were glaucoma suspects, ocular hypertensives, stable/early/moderate POAG, PXF, Pigmentary Glau, px who can perform vf examinations, VA of 6/18 or better both eyes. People who are excluded - unstable glau, normal tension, 2ary glaus, narrow angle glau, any other existing ocular pathology, advanced VF loss and best corrected VA of 6/18 or less.

There was a study from 1993-1997 which showed that the optom and HES measurements were equally reliable and outcomes were comparable after two years of review. Px were more satisfied with having the check done at the local optom presumably because it was closer/easier to get to. The full cost of the assessments was cheaper if everyone was done at the hospital though. So after this study the scheme wasn't introduced. There was increased involvement of in house optoms within the Bristol eye hospital though

Glaucoma Mega Brief Version

Progressive optic neuropathy associated with elevated IOP. Has characteristic field defects - nasal step, arc scotoma etc. Lowering IOP is protective even in normal tension glau.

Fluid in the eye is produced and drained away at a certain rate. Glaucoma doesn't involve a problem with increased production, it's a drainage issue. You can help by lowering the production though. Normal IOP is considered to be 21 or less. Ocular hypertension is when pressure is higher than normal but the px doesn't have glaucoma. There's a diurnal fluctuation - usually higher in the AM.

Goldmann/Perkins is used if optom is unsure whether to refer or not. History can give clues - hyperopes are more prone to closed angle glaucoma whereas myopes are more prone to open angle. If the patient has had refractive surgery then the change in rigidity/flatness of the cornea could lead to underestimation of the pressure. Also side effects of asthma treatment could increase chance of glau.

Damage may progress as follows - if some nerves are damaged then the surrounding nerves can follow. It's thought that using some drugs the surrounding nerves can be spared. Research into this is in progress the noo.

The optic disc is imaged mostly with the direct ophthalmoscope but indirect biomicroscopy is becoming more widespread in practice. Also fundus photography, stereo imaging and computerised topography. Disc assessment concerns the cup and disc size. The disc should follow the ISNT rule, if it doesn't then suspect glaucoma. The NRR should be thickest at the inferior, then superior, then nasal, then temporal. Also look for focal loss of ON fibre tissue and disc haemorrhages.

Assessment of the anterior chamber angle can be with Van H's on the slit lamp, ultrasound, Gonioscopy - shaffer grades.

There are various types of glaucoma - open and closed/narrow angle, chronic and acute, primary and secondary, congenital, juvenile and adult.

With pseudoexfoliative glaucoma small flecks of white material are noticed in the pupil (on the edge of the lens). They are very easily seen if the pupil is dilated. Other types include pigmentary, uveitic, steroid induced and rubeotic.

Angle Closure glaucoma assessment. As I typed before closure is more likely in a hypermetropic patient. Ask if any headaches/intermittent blurred vision, haloes around lights (corneal oedema), whether taking anti-deps, drugs for asthma etc. If px has IOP of 60 or something could do gonioscopy, instil pilo, acetazolamide, peripheral iridotomy, surgery (trabeculectomy/lens extraction)

Angle closure typically involves small eyes, a mid-dilated fixed pupil, iris atrophy, ON cupping/field loss

Normal Tension Glaucoma - 10-30% of glaucomas are actually normal IOP. This is mostly older PX. If you can lower pressure more still by using medication or surgery then you can slow down progression.

Pilocarpine causes constriction of ciliary muscle fibres, opens trabecular meshwork, increases outflow, causes miosis, headache and low vision in dim light, also contributes to myopia, cataract and accommodative spasm. Instilled 4x/day

Adrenergic type drugs like epinephrine increase aqueous drainage. They can cause adrenochrome deposits (black granules in conj), mydriasis (angle closure glau), rebound hyperaemia and allergic reaction

Alpha-2 agonists like apraclonidine are not often used. They decrease production and increase drainage but cause dry mouth, allergy, headache and fatigue.

Beta Blockers - beta receps in eye moderate aq production so blockers decrease secretion. They become less effective over time and can cause bronchospasm which in asthma px could actually cause respiratory failure and even death if given enough drops. Preps inculde timolol, betaxolol

Prostaglandins increase outflow via trabecular and uveoscleral routes. eg latanoprost. 50% of px are on this. Can cause increased iris pigmentation, thicker eyelashes and hyperaemia. It's expensive too.

Carbonic Anhydrase Inhibitors like acetazolamide are used in the short term for px w/uveitis. Side effects include nausea, lethargy, metallic taste, kidney stones, all. reaction. Combos of the above are also used.

Surgery could involve iridotomy, iridectomy, laser trabeculoplasty. Probs include plain old failure of it to work, accelerated cataract, endophthalmitis

Shared Care: Optometric Management of Glaucoma

The glaucoma prevalence for europeans - one percent of ages 40-60, 2% of over 60s and >3% of those over 80. The risk factors are as follows

• Age, gender (F), race (african/afro-carribean)
• IOP, ON Head, Myopia/Hypermetropia
• Diabetes, systemic hypertension
• Family History (FH)
• Smoking, alcohol, socio-economic factors

If IOP is less than 15 glau is very unlikely. Anything between 15 and 25 is low tension. 25 upwards the risk of POAG goes up from 10% to about 35%

People with high diurnal variation are more likely to have glaucoma also. A glaucoma patient also has poor VA in mid range contrast sensitivity. You wouldn't normally spot this as most optoms just use a normal snellen w/high contrast. You could spot it w/a pelli robson though. Blue/Yellow fields are more sensitive when spotting the early visual loss.

There is ganglion cell damage in glaucoma. There are two theories behind this

1. Magno vulnerability where selective loss of magno cells (concerned w/good flicker/motion perception and more sensitive to low contrast stuff
2. Redundancy whereby magno and parvo cells are lost at the same rate but the larger number of parvo cells means the effect is less pronounced at high contrast

Glaucoma Management Pathway

1. Patient attends optom, has sight test. IOP = >21 w/applanation tonometry and/or vfd and/or suspicious discs. This results in the patient/optom making an appointment with an optom with a specialist interest in glaucoma or an OMP
2. Px attends that person and a full assessment is carried out according to protocol. A decision is taken whether the patient has ocular hypertension (OSI/OMP reviews) or can be discharged (return to optom) OR has glaucoma (treat or refer to HES). The px is advised and given further info
3. OSI/OMP relays data to HES and the HES reviews the data, advises regarding management and sets up review at HES if needed
4. OSI/OMP manages px in community setting w/regular reviews set in place. OSI/OMP relay data to the hospital if there's significant progression for HES review if req

Each different shared care scheme has its own recruitment, testing and re-referral criteria. Varies. eg Bristol - people who are included have stable POAG, pigmentary or pseudoexfoliative glaucoma but other glaucomas (ie stuff that needs surgery) is going to be excluded.