NOTES:

• My notes are in blue.

• The order of the lecturer’s notes was rearranged slightly to reflect the order of
presentation.
• The sections without any additional notes were not discussed in class. I’m assuming we
are still responsible for them…
–GF

For more information on diseases, Dr. Shaw recommended Google.

Retinal Diseases:
• Retinal disease have many age- and lifestyle factors. NDs can have an impact on these
conditions.
Age Related Macula Degeneration
Retinal Detachment
Diabetic Retinopathy
Inherited Disorders (retinitis pigmentosa, achromatopsia, albinism…)
Histoplasmosis, Toxoplasmosis

Diabetic Retinopathy
More common with long standing type 1 diabetics and non-compliant type 2’s (in as little as a
year)
Treatment with laser photocoagulation
Early intervention necessary
Regular checkups mandatory
Keep blood glucose within target
• Diabetes has an effect on the basal membrane of blood vessels in the eye.
• If Db is poorly controlled, there is a much higher incidence of systemic disease like diabetic
retinopathy (occurs in eyes, but other BV too)
• Have to educate patients to control blood sugar with diet, insulin
• All diabetics need to have regular eye exams
• Should photograph retina to monitor changes.
• Laser can be used to decrease effect of blood leakage.
• Sequelae: blindness, kidney disease. Have to help pt. maintain blood sugar levels.
• If blood vessel breaks, get aneurysm, hemorrhage. Will see cotton wool spots on retina.
Need to refer if we see this in patient.

Macula Degeneration (Age related macular degeneration: ARMD)

• Common. Large lifestyle component
• Caused by decreased ability of retinal tissue to take light energy and convert it to neural
discharge.
• High metabolism in retinal tissue: needs large supply of oxygen, carbs
• When supply decreases, the retina starves. Responds to decreased supply.
• Body tries to compensate by growing new blood vessels, or shuts tissue down. Decreased
supply due to normal aging.

DDX LECTURE 8, OCTOBER 11TH – PAGE 1

• If we can provide these nutrients (diet), we may be able to slow ARMD)
Reduced permeability of Bruch’s Membrane
Insufficient nutrients available to sensory tissue
Limited to central, macula region due to anatomy of circulation
Resultant central vision loss
Damage from visible radiation(light)
Macular Degeneration: Risk factors
Tobacco: 50% risk factor?
• Nicotine causes constriction of peripheral blood vessels which may decrease the available
nutrients. Not everyone who smokes get MD, but 50% of smokers do.
Inherited risk + Northern peoples living in less northern regions
Diet factors
• Eating foods that increase damage to blood vessels: hydrogenated vegetable oils, foods that
create free radicals, pollution. “not everything that you eat is food!” Many additives to our
foods: salts, sugars, preservatives, convenience foods.
Excessive exposure to light
Wear sun glasses
Nutrition and treating ARMD
Lutein supplements: Proven effective >6mg/day
Zinc > 80 mg/day

LAST study, Optometry 2004;75:216-30)

Anti oxidants Not proven
Green vegetables: Brocolli, Spinach etc
Orange vegetables: Contain lutein: squash, yam,
Omega 3 fatty acids
Avoid saturated fats and Hydrogenated oils (are they even edible?) Probably a risk factor
• Blood type may be a factor
• Heritage? More common with fair skin.
• Can help prevent disorder by knowing risk factors.

• Bioflavonoids: proteins and dyes (natural). Seem to help prevent MD.

• Study done by drug company found that lutein and zinc can be helpful. Beta carotene may
reduce absorption of lutein
• Lutein: pigment that makes plants dark: blueberries, kale, blackberries.
• Zinc: need 80mg dose (only 10mg in Centrum)

Posterior Vitreous Detachment

• The vitreous is a gel that occupies the space between the lens and the retina. Keeps the shape
of eyeball. Shock absorber for trauma.
• Holds retina in place (not fixed to back of eye)
• Clear, gelatinous vitreous is healthy. Can become less homogenous, lumpy, starts to shrink.
Patient will start to see floaters.
• Often >50 years

DDX LECTURE 8, OCTOBER 11TH – PAGE 2

• Might start to see “squiggly things” with opthalmoscope
• When vitreous shrinks, might pull retina away from eye.
• When the retina moves, gives off FLASH to brain. Sense of seeing something in front of eye
• Should refer right away to eye doctor.
Differentiate from Retinal Detachment
• We can’t see the difference between vitreous and retinal detachment. As vitreous detaches, it
may not take the retina with it at first.
• Vitreous may TEAR the retina as it detaches. If the retina tears, the vitreous will leak
through and detach the retina, like wallpaper peeling off a wall. It is important to fix tear
ASAP. Better chance of repair, recovery.
• Detached retina can happen up to 2 weeks after detachment of vitreous. PVD is major cause
of idiopathic retinal detachment.
• ***MUST REFER PVD SO IT CAN BE TREATED BEFORE IT BECOMES DETACHED
RETINA!!!***
Symptoms Flashes and floaters. Patients often describe a net in front of their eyes
Flashes at location of current separation (like sparks)
Vitreous shrinks and detaches from the posterior pole/retina

Commonly occur in over 60% after age 50

“Physiological” due to change in protein structure of the vitreous
Need dilated fundus exam to rule out retinal hole or tear that could precipitate a retinal
detachment.
May be an emergency
Refer to optometrist then he/she will refer to retinal surgeon if necessary

Detached Retina

Urgent care required

Time of the essence
Treatment with surgery
More common in age 40 +
Associated with trauma
• People who are near-sighted are more likely to have detached retina than people who are far-
sighted.
• Near-sighted: larger eyes, less stable, more fragile. Smaller eyes tend to be tougher than
larger ones.
• If near-sighted, may be more adhesions of retina, therefore more tears if the vitreous
detaches.
• Poke in eye? Increases chance of retinal detachment. Other trauma: car accidents and sports
injuries increase chance.
• Diabetes: If there is bleeding into vitreous, there will be scarring in vitreous, may pull off
retina.
• Posterior vitreous detachment on its own is benign. Patient will see flashes of light. This
isn’t a detached retina, but it could be within 2 weeks.

DDX LECTURE 8, OCTOBER 11TH – PAGE 3

Retinal Tear

High risk of detachment

May be secondary to posterior vitreous detachment
Hard to see
Visual acuity reduced

Symptoms of a flash:
• Based on patient’s report of symptoms. No lab tests to confirm.
• What do the symptoms mean? What is a flash?
Associated with detachment of vitreous
Very short duration. Spark.
Like mechanical flash (from trauma): Sudden flash: instantaneous.
• Longer-term problems:
Aura, zig-zag vision: like mirage off hot pavement.
Lasts seconds to minutes.
Temporary vision loss.
Usually in both eyes. Something is interfereing with the blood to visual cortex, reduced
circulation to optic nerve.
Headache may follow.

Migraine Headache
• From food allergies, caffeine, weather. Patients may have an aura: semi-circular pattern.
Prodrome of migraine.
• Don’t have to have a headache with a migraine! May just have visual disturbance, which is a
“silent migraine”.
• Can be transient ischemia (d/t embolism), high blood pressure.
• Persistent transient ischemia in patients over 40? Get full blood work done. Systemic
problem.
• Carotid artery disease: blood supply to brain is compromised. Vision loss on contralateral
side.
• (Look at maps of visual fields in PCD book to find out what parts of visual field are affected
by different blockages.)
• Bilateral visual distortion from ischemia will be on the same side of both eyes (eg. The right
side of the visual field in both eyes)
• Strep infection => rheumatic fever: causes vegetative growth on mitral valve. This can
release emboli into circulation, may cause persistent transient ischemia leading to vision loss.
• Transient ischemic attack: have to figure out if patients are having this because of migraine
(constricted BV) or due to a systemic problem (eg. CV)

Papilledema
Elevated intracranial pressure (in ventricles of brain)
• Puts pressure on optic nerve.

DDX LECTURE 8, OCTOBER 11TH – PAGE 4

• When looking at optic nerve, we get a view into the brain tissue, and the status of blood
vessels in the body.
• If you see an elevated or fuzzy optic nerve head, this may be papillodema. Refer to
neurologist.
• Could be psudotumour cerebri (he didn’t explain what this was). Most common in 25-50
year olds who are slightly overweight females.
• Mimics tumour: swelling in brain. Treat with Diamox-sucks water out of brain (osmosis)
• Unknown cause: are the patients slightly overweight because they are holding water in other
parts of the body as well?
MRI or CT to confirm etiology
Differentiate from optic disc drusen
Tumour?

Toxoplasmosis
< Active
Intracellular protozoan: Toxoplasma gondii
undercooked meat and dairy products
indirect ingestion of cat feces
< Inactive
• Protozoa in cat and raccoon feces. Keep kids and pregnant women away from cat litter!
Teratogenic in pregnancy!
• Protozoa likes to go to retina of 1 eye only
• Also contracted from undercooked pork. Common in small mammals.
• Doesn’t cause total blindness, but scars retina
• Will see big white hole in retina with pigment around it.

HistoplasmosisHistoplasma Capsulatum
Retinal disease
An affinity for choroidal tissue
Granulomatous inflammatory masses that disrupt Bruch's membrane
Fungal inflammation from bird droppings
• Fungal infection: inhaled with dried bird droppings.
• Risk for chicken farmers, restoration work on buildings where pigeons have been roosting.

Albinism
Autosomal recessive (Oculo-cutaneous) or X linked (ocular & O-C)
hypoplastic macula
pendular nystagmus
Lack of retinal pigment, pigment is very transparent. Doesn’t catch as much light, therefore,
their vision is less acute.
1/20,000 prevalence
Vision Impaired

Retinitis Pigmentosa
Loss of night vision (nyctalopia) as well as

DDX LECTURE 8, OCTOBER 11TH – PAGE 5

Loss of peripheral vision.
Autosomal dominant, autosomal recessive, X-linked, simplex, multiplex),
Often vision impaired
Endpoint often total blindness
• Age-associated

Retinal Artery Occlusion

Sudden painless vision loss
pale, milky, edematous retina
. An embolus may be visible in the vasculature on the disc or at a branch
• Artery occluded by embolus. Not blood getting into retina from inside. Some comes from
exterior supply, but it isn’t enough.

Retinal Vein Occlusion

Usually elderly, Hx diabetes and hypertension.
Asymptomatic? sudden painless unilateral loss of vision and/or visual field?
• Vein is blocked, blood can’t get out.
• Can happen from occlusion by nearby artery. If artery is hardened, or in hypertension, artery
can squeeze vein shut.
• Systemic rather than eye disease. Increased risk of secondary event (CV disease)
• Patients with this problem probably have other health problems.

AIDS and the eye

is a multi-system disorder of opportunistic infections caused by the human immunodeficiency
virus (HIV).
Often the eye suffers Cytomegalovirus (CMV).
• If patient is healthy, CMV is not a big deal.
• If immunocompromised, more cause for concern.
• Watch for patients that have continuous or unresolved health problems. They may be
immunocompromised and not realize it.

Understand this material for the quiz:

• Urgency of referral: what needs to be referred?
• The eye lets us know when things are wrong: PAIN!
• Painful eye? The cornea is usually involved. Foreign body? Ulcer?

• Red eye with no pain? Probably not an emergency.

• Lots of nasty discharge? Infection.
• No nasty discharge? Probably not an infection.
• Questioning patient helps diagnose. Understand their chief concern when taking their history
and focus your questions on this.

• #1 problem with patients is “gritty eyes” (dry eyes). There are supplements that we can
prescribe to treat dry eyes.

DDX LECTURE 8, OCTOBER 11TH – PAGE 6

• Differentiate between chronic and acute conditions.
• Sudden onset of blurriness? Refer.
• Gradual, long-term onset? Probably not as urgent.

• Young kids tend to get viruses that turn into bacterial infections (I think…) URTI too. Think
about patient’s lifestyle to help diagnose.

• Transmission of virus is more likely to go into body through the nose than through the
mouth.
• Sudden vision loss? Deal with this quickly.
• Poor hygiene and diet mean that patient is at higher risk for a lid infection.

Glaucoma: Chronic open angle

Typically inherited dominant trait
50% chance if 1 parent
May be steroid induced
Incidence increases with higher intraocular pressures
Atrophy of the optic nerve perhaps due to decreased micro circulation
All must be screened routinely
More prevalent 35+
• If chronic, may be asymptomatic. Treated with medication, surgery. Should be treated
within 2 years.
• If acute, urgent treatment required. Hazy vision, fixed large pupil, patient is uncomfortable.
Very high pressure on eyeball, needs to be treated within hours.

Primary Open Angle Glaucoma (this is the same thing as chronic open angle)
Treated with Topical and systemic meds, laser and or surgery
Long term meds have with side effects: depression and impotence
Gradual loss in vision if not treated

3rd Cranial nerve palsy

Sudden onset unilateral ptosis (droopy eyeid)
If from ischemic vasculopathy will spontaneously resolve and recover over a period of three to
six months

4th cranial nerve palsy

Sudden vertical diplopia
frequently concurrent hypertension and/or diabetes.
40 percent of all isolated fourth nerve palsies are traumatic, 30 percent are idiopathic, 20 percent
are due to vascular infarct, and only 10 percent are due to tumor or aneurysm.

6th Cranial Nerve Palsy

often self-correcting, but indicator of diabetes or HT.
Sudden onset horizontal Diplopia

DDX LECTURE 8, OCTOBER 11TH – PAGE 7

Typically an adult over 50 with an isolated sixth nerve palsy require a workup for ischemic
vascular diseases such as diabetes and hypertension.
One eye cannot turn out (abduct). Lateral rectus stops responding.
Can self correct, may need a prism on one eye
DDX Myasthenia gravis

Myasthenia gravis
autoimmune disease
destroys key components of the neuromuscular system responsible for governing muscular
activity.
Variable diplopia!
Patients should always be educated to report difficulties with breathing or swallowing.

Graves Disease
Exophthalmos
a multi-system disorder
unknown etiology,
hyperthyroidism associated with diffuse hyperplasia of the thyroid gland;
infiltrative ophthalmopathy;
infiltrative dermopathy (pretibial myxedema).

Exophthalmos due to increase in thickness of extra ocular muscles

Horner's syndrome
interruption of the oculosympathetic nerve pathway somewhere between its origin in the
hypothalamus and the eye.
ptosis,
pupillary miosis
facial anhidrosis

Eye Care

Optometrist: Primary referral

Ophthalmologist: Eye Surgeon and sub specialist
Family Physician: limited knowledge for treatment
References:
http://www.revoptom.com/handbook/hbhome.htm
Review of optometry
Lecturer: Dr Peter Shaw O.D.
Scarborough Low Vision Centre
3030 Lawrence Avenue East 416 438 3525
5915 Leslie Street 416 494-3050

DDX LECTURE 8, OCTOBER 11TH – PAGE 8