Lecture 8 Oct 11th

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 farsighted. • 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.

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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.

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#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

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

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

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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.

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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

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