L24 Nervous System Clinical Ophthalmology

Overview

A whole-class clinical ophthalmology lecture covering why vision matters and how blindness is defined and counted (globally and in New Zealand), the anatomy of the eye as seen on examination, the core bedside eye examination, the four refractive errors, and the main causes of vision loss (cataract, glaucoma, age-related macular degeneration, diabetic retinopathy) with their presentation and treatment. It closes with a short “what can we see in the eyes?” section on systemic disease and pupil abnormalities.

Importance of vision

• 80% of our sensory input comes through our eyes.
• Vision underpins navigation and safety, learning and education, communication (facial expressions, body language), social interaction and relationships, appreciating the world (nature, art), independence and functionality (working), and health and wellbeing.
• Vision loss is associated with a higher risk of mortality, falls, accidents, depression and dementia:
  • 1.5 to 2 times the risk of falls
  • 4 to 8 times the risk of hip [see warning below]
  • 3.5 times higher depression
• Survey of what Americans would most miss seeing if they lost their vision: loved ones’ faces 37%, children’s milestones 26%, nature 23%, pets 22%, favourite TV shows/movies 15%.
• Annual eye exams in children: 1 in 4 children has a vision problem; 60% of children with learning difficulties have an undetected vision problem; 80% of information children receive in the classroom is presented visually; 70% of juvenile delinquents have an undetected and untreated vision problem. Vision also affects sports performance through hand-eye coordination, depth perception and eye tracking ability. Message: every child, every year.

Warning

The slide text for the hip risk figure is cut off (“x 4-8 times risk of hip”), so the endpoint is not stated in full on the slide.

Defining blindness and visual impairment

Blindness is distinguished from visual impairment using two measures.

• Visual acuity, expressed as a Snellen fraction:
  • Metric: 6/6 or 4/4
  • Imperial: 20/20
• Visual fields: vertical 135 degrees, horizontal 180 degrees.

WHO definitions:

• Blindness: worse than 3/60, or less than 10 degrees of central vision, in the better eye, with correction.
• Visual impairment:
  • Mild VI: worse than 6/12 to 6/18
  • Moderate VI: worse than 6/18 but better than or equal to 6/60
  • Severe VI: worse than 6/60 but better than or equal to 3/60
  • Low vision (VI): 6/18 to 3/60, less than 20 degrees central vision

Epidemiology of blindness

Global

• Low vision 246 million; blindness 39 million.
• 50% of vision loss is cataract.
• Causes worldwide: cataract 51%, uncorrected refractive errors 17%, glaucoma 8%, AMD 5%, diabetic retinopathy 5%, other causes 5%, corneal opacities 4%, childhood blindness 4%, trachoma 1%.

New Zealand

• Low vision 125,000, of whom 12,000 are Maori.
• Cost $22,217perperson,totalling$2.8 billion; $198 million in direct health costs alone.
• Causes of blindness among New Zealanders aged 50 or over (2009): AMD 48%, glaucoma 16%, cataract 11%, uncorrected refractive error 3%, other 21%. Note the contrast with the global picture, where cataract dominates.
• Blind Foundation registrations in NZ (2016), 12,272 people: by age, 80 years and over 5,948 (48%), 22 to 64 years 3,301 (27%), 65 to 79 years 1,908 (16%), 0 to 21 years 115 (1%); by sex, women 7,229 (59%), men 5,043 (41%).

What can be done

• 80% of vision loss and blindness is preventable or treatable.
• The main issues are access, awareness, and funding/cost.

Eye anatomy

Structures labelled on the cross-section of the eye: cornea, anterior chamber, iris, pupil, posterior chamber, lens, zonules, ciliary body, canal of Schlemm, vitreous body, retina, choroid, sclera, fovea, optic disc, optic nerve (cranial nerve II), and the central retinal artery and vein.

On examination:

• Cornea and lens are assessed for opacity: a cloudy grey cornea with a dark lesion (corneal opacity) and a cloudy white lens (cataract) were shown as clinical examples.
• Retina on fundus photography: retina, optic nerve, fovea, and the macula (the region surrounding the fovea).
• Optic nerve: the optic disc varies between individuals in colour and in cupping.

Warning

The cornea/lens and optic disc slides are photographs with no text labels, so the slides do not state which findings are normal and which are abnormal.

Eye examination basics

• Vision (visual acuity): Snellen chart. Top line is 6/60. At 6/12 many social activities are possible, and this is the UK driving test standard. 6/6 is “normal” eyesight, also known as 20/20 vision.
• Visual field: confrontation testing, with the patient covering one eye while the examiner presents fingers in the periphery.
• Eye movements: test the nine cardinal directions of gaze.
• Pupil reaction: compare the pupils with no light, the normal constriction response to light, and a positive relative afferent pupillary defect (RAPD), in which the affected eye fails to constrict appropriately when light is directed at it.
• Direct ophthalmoscopy, including the blue/cobalt filter with fluorescein staining, which shows green staining where there is a corneal surface defect such as an abrasion.
• Slit lamp examination.
• Pressure: tonometry for intraocular pressure, with the patient’s forehead against a headrest.

Refractive errors

• Myopia (near sightedness): light rays converge in front of the retina; corrected with a concave (minus) lens.
• Hypermetropia (far sightedness): light rays converge behind the retina; corrected with a convex (plus) lens.
• Astigmatism: the cornea is oval rather than spherical, so there are multiple focal points instead of one. Patients notice streaky, starburst lights, classically when driving at night.
• Presbyopia: the image focuses behind the retina for near work, so objects are held at arm’s length. Understand it against normal accommodation:
  • Far objects: ciliary muscle relaxed (increased diameter), zonules tight, lens flatter.
  • Near objects: ciliary muscle contracts (decreased diameter), zonules relaxed, lens increases in convexity. This is accommodation.

Cataract

• Opacification of the lens, seen as a cloudy or opaque lens through the pupil; appearances range from dense yellow-brown to blue-tinted to a dark central opacity seen against the red reflex, and dark streaks on retro-illumination.
• Symptomatically it produces a blurred, out-of-focus image compared with normal vision.
• Treated surgically: incision at the cornea/limbus, capsulorhexis of the anterior lens capsule, phacoemulsification and removal of the lens material, then insertion of a clear intraocular lens. Patients leave with an eye patch or shield.
• Recap points for the non-specialist: awareness; identification and effect on quality of life; check the red reflex; exclude other pathology; remember refraction.

Warning

The cataract image slides carry no labels distinguishing cataract types, so type-specific detail is not available from the slides.

Glaucoma

• A progressive optic neuropathy with a specific visual field defect.
• Intraocular pressure has a common role: it may be high (20 mmHg) or normal, and lowering IOP slows progression.
• Monitored both structurally and functionally: OCT retinal nerve fibre layer thickness maps for each eye, alongside serial visual fields, which are reported over time as “possible progression” then “likely progression”.
• Optic disc appearance (cupping) is the clinical sign shown on fundus photographs.
• Treatment
  • Medical, topical: prostaglandins, beta-blockers, alpha-agonists, carbonic anhydrase inhibitors.
  • Laser.
  • Surgical.

Age-related macular degeneration

• Dry AMD: 90% of cases, chronic, no treatment. Features are drusen and pigmentary change, and geographic atrophy on the paired fundus/OCT images.
• Wet AMD: 10% of cases, acute, treatable. Features are subretinal fluid, haemorrhage and fibrosis.
• Symptoms: decrease of vision, central scotoma, distortion. The patient’s experience is a clear peripheral image with the central area blurred and distorted.
• Amsler grid: normal shows straight lines around a central fixation dot; in AMD the lines are wavy (metamorphopsia) with a dark area near the centre (central scotoma).
• Treatment of wet AMD: anti-VEGF intravitreal injections, one a month initially, later extended depending on the response.
• Recap points: awareness of distortion; specific symptoms of central vision; risk factors are age and smoking; anti-VEGF injections.

Diabetic retinopathy

Classification and progression

1. No clinical retinopathy.
2. Mild NPDR: microaneurysms only (localised swelling of small blood vessels).
3. Moderate NPDR: more than microaneurysms but less than severe NPDR; mild NPDR plus dot and blot haemorrhages, hard exudates or cotton wool spots.
4. Severe NPDR: more than 20 intraretinal haemorrhages in each of 4 quadrants, venous beading in 2 or more quadrants, IRMA (intraretinal microvascular abnormalities) in 1 or more quadrant, and no signs of PDR.
5. PDR: new vessels elsewhere and/or around the disc, and/or preretinal or vitreous haemorrhage; also tractional retinal detachment and fibrous proliferations.

The ETDRS-DRSS levels map onto this: levels 35/43 mild to moderate NPDR, levels 47/53 moderately severe to severe NPDR, levels 60 to 75 moderately severe to severe PDR.

Risk of progression from NPDR to PDR

• Mild NPDR: 5% or less
• Moderate NPDR: 12 to 27%
• Severe NPDR: 50%

Risk factors for progression: poor blood sugar control (high HbA1c), high blood pressure, high cholesterol, smoking and other lifestyle factors, and duration of diabetes (longer duration increases risk).

Prevalence of PDR by diabetes type

• Type 1 (DM1), 5 to 10% of people with diabetes: after 10 years 25%, after 20 years 50 to 60%, after 30 years 75 to 90%.
• Type 2 (DM2), 90% of people with diabetes: after 10 years 5 to 10%, after 20 years 15 to 25%, after 30 years 40 to 50%.
• DM1 shows faster and higher progression to PDR because of early onset and longer duration; DM2 progresses more slowly and patients are diagnosed later.

Proliferative disease is recognised on fundus photography by abnormal new vessels near the optic disc and elsewhere in the retina.

Treatment of PDR: laser photocoagulation (leaving scattered scars across the peripheral retina) and anti-VEGF injections.

Diabetic macular oedema

• Seen as yellow-white hard exudates in a circinate pattern near the fovea.
• Prevalence: DM1 (5 to 10% of people with diabetes), after 10 years 10 to 15%, after 20 years 20 to 30%, after 30 years 30 to 40%. DM2 (90%), 3 to 10% at the time of diagnosis because DM2 is diagnosed later, after 10 years 10 to 15%, after 20 years 20 to 25%, after 30 years 30 to 40%.
• Risk is influenced by glycaemic control (HbA1c), high blood pressure and dyslipidaemia.
• Treatment: anti-VEGF injections, one a month and later extended depending on the response; also steroids, and less laser.

Recap points: your role is regular checkups and glycaemic and blood pressure control; diabetic retinopathy screening; identify retinal changes and vitreous haemorrhage.

Patterns of presentation

The lecture groups the four major diseases by how vision is lost.

• Gradual and painless: cataract, glaucoma, diabetic retinopathy, age-related macular degeneration.
• Sudden but painless: the same four conditions are listed again under this heading as each is introduced (AMD and diabetic retinopathy in turn).

Other retinal pathology

Briefly shown under “others”: diffuse mottled pigmentary change, retinal tear and retinal detachment (illustrated both as a cross-sectional diagram and on fundus photographs), and a small round reddish retinal lesion.

What can we see in the eyes: systemic disease

A closing image-based segment titled “Systemic diseases in the eyes”, presenting unlabelled clinical photographs for interpretation:

• yellowish/pigmented discolouration of the conjunctiva/sclera near the limbus
• scattered yellow-white exudates and small haemorrhages at the posterior pole
• marked conjunctival injection around the iris with a slightly irregular pupil
• a large, well-demarcated darkly pigmented lesion at the posterior pole with vessels crossing it
• a cloudy opacity within the pupil with a small white structure adjacent near the iris
• a pale/pink optic disc with a faint reddish retinal patch
• a localised bright red subconjunctival haemorrhage
• a cloudy, greenish/hazy cornea with conjunctival injection
• extensive bright red haemorrhage covering most of the visible conjunctiva/sclera

Warning

None of these systemic-disease images carries a diagnosis on the slide, so the specific conditions they illustrate cannot be recovered from the slides alone.

Pupil appearances

Three compared side by side:

• Normal pupils: both equal in size.
• Dilated pupils: both enlarged and equal.
• Anisocoria: unequal pupil size between the two eyes.

Self-test

1. State the WHO acuity and visual field criteria for blindness.
2. List the four WHO grades of visual impairment with their acuity ranges.
3. What acuity is the UK driving test standard, and what does the top line of the Snellen chart represent?
4. What are the normal extents of the visual field, vertically and horizontally?
5. Distinguish the leading cause of blindness worldwide from the leading cause among New Zealanders aged 50 or over, giving the percentage for each.
6. What proportion of vision loss and blindness is preventable or treatable, and what three issues stand in the way?
7. Describe the changes in the ciliary muscle, zonules and lens when the eye focuses on a near object.
8. Distinguish myopia from hypermetropia by where light converges and by the corrective lens used.
9. Explain why astigmatism produces starburst lights at night.
10. Describe what a positive RAPD looks like on the swinging light test.
11. What does fluorescein staining under blue light demonstrate?
12. Describe the steps of cataract surgery in order.
13. Define glaucoma, and explain the role of intraocular pressure in it.
14. List the four topical drug classes used in glaucoma.
15. Distinguish dry from wet AMD by frequency, course, features and treatment.
16. What three symptoms does macular degeneration produce, and what does the Amsler grid show in a patient who has them?
17. State the criteria for severe NPDR.
18. What distinguishes PDR from severe NPDR?
19. What is the risk of progression to PDR from mild, moderate and severe NPDR?
20. Explain why type 1 diabetes progresses to PDR faster and more often than type 2.
21. List the risk factors for progression of diabetic retinopathy.
22. Describe the treatment of diabetic macular oedema.
23. Distinguish normal pupils, dilated pupils and anisocoria.
24. A 78-year-old reports that straight lines look wavy and that the centre of her vision is missing, with the periphery intact. Which condition does this suggest, which subtype, what bedside test would you use, and what treatment is available?
25. Two patients each have painless gradual vision loss: one has a cloudy lens on red reflex testing, the other has a normal anterior segment but progressive peripheral field loss on serial testing. Explain which disease each has and how the mechanism of vision loss differs.

Answers

Reveal answers

1. Worse than 3/60, or less than 10 degrees of central vision, in the better eye, with correction.
2. Mild VI worse than 6/12 to 6/18; moderate VI worse than 6/18 but better than or equal to 6/60; severe VI worse than 6/60 but better than or equal to 3/60; low vision 6/18 to 3/60 with less than 20 degrees of central vision.
3. 6/12 is the UK driving test standard, at which many social activities are possible. The top line of the chart is 6/60.
4. Vertical 135 degrees, horizontal 180 degrees.
5. Worldwide the leading cause is cataract at 51%; in New Zealanders aged 50 or over it is age-related macular degeneration at 48%, with cataract only 11%.
6. 80% is preventable or treatable. The main issues are access, awareness, and funding/cost.
7. The ciliary muscle contracts and its diameter decreases, the zonules relax, and the lens increases in convexity. This is accommodation.
8. In myopia rays converge in front of the retina and are corrected with a concave (minus) lens; in hypermetropia rays converge behind the retina and are corrected with a convex (plus) lens.
9. The cornea is oval rather than spherical, so light is brought to multiple focal points instead of one, producing streaky, starburst images from point lights.
10. With light directed at the affected eye the pupil fails to constrict appropriately, whereas the normal eye constricts to direct light.
11. Green staining of the corneal surface under the blue/cobalt filter, indicating a corneal epithelial defect such as an abrasion.
12. Incision at the cornea/limbus; capsulorhexis of the anterior lens capsule; phacoemulsification of the lens material; removal of the remaining lens material; then insertion of a clear intraocular lens.
13. A progressive optic neuropathy with a specific visual field defect. Intraocular pressure has a common role: it may be high (20 mmHg) or normal, and lowering it slows progression.
14. Prostaglandins, beta-blockers, alpha-agonists, carbonic anhydrase inhibitors.
15. Dry AMD is 90% of cases, chronic, with drusen, pigmentary change and geographic atrophy, and there is no treatment. Wet AMD is 10%, acute, with subretinal fluid, haemorrhage and fibrosis, and is treated with anti-VEGF injections.
16. Decrease of vision, central scotoma and distortion. The Amsler grid shows wavy, distorted lines with a dark or shaded area near the centre, instead of the normal straight lines around a central fixation dot.
17. More than 20 intraretinal haemorrhages in each of 4 quadrants, venous beading in 2 or more quadrants, or IRMA in 1 or more quadrant, with no signs of PDR.
18. PDR shows new vessels elsewhere and/or around the disc, and/or preretinal or vitreous haemorrhage, with fibrous proliferation and tractional retinal detachment; severe NPDR has none of these new-vessel signs.
19. Mild NPDR 5% or less, moderate NPDR 12 to 27%, severe NPDR 50%.
20. Because of its early onset and therefore longer duration of disease; type 2 progresses more slowly and those patients are diagnosed later.
21. Poor blood sugar control (high HbA1c), high blood pressure, high cholesterol, smoking and other lifestyle factors, and longer duration of diabetes.
22. Anti-VEGF injections, one a month and later extended depending on the response, plus steroids and less laser.
23. Normal pupils are equal in size; dilated pupils are both enlarged but still equal; anisocoria is unequal pupil size between the two eyes.
24. Age-related macular degeneration, wet subtype (acute and treatable, with subretinal fluid, haemorrhage and fibrosis); test with the Amsler grid, which will show wavy lines and a central dark area; treat with anti-VEGF intravitreal injections, monthly at first and later extended depending on response. Her risk factors would be age and smoking.
25. The first has cataract, where the lens itself opacifies and blurs the whole image, and it is corrected by removing the lens and implanting an intraocular lens. The second has glaucoma, a progressive optic neuropathy in which the visual field is lost from the periphery while the media stay clear; it is monitored with serial visual fields and OCT nerve fibre layer thickness, and treated by lowering intraocular pressure medically, by laser or surgically.