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Flashcards in Optho Deck (118):

Layers of eye

Fibrous tunic (sclera, cornea)
- Corneo-scleral layer

Vascular tunic (iris, ciliary body, choroid)
- Choroid (uveal) layer

Retina (pigmented, neural layers)
- Retinal layer with nuclei lined up in pigmented layer (outermost layer abutting choroid layer)
- Retinal pigmented layer= Cells also have phagocytic components to clean up retinal cells that turn over


Chambers of eye

Anterior chamber=
- Space defined by cornea, iris, lens
- Filled with Aqueous humor

Posterior chamber=
- Spaced defined by iris, lens, zonule fibers, ciliary body
- Filled with aqueous humor

Vitreous chamber=
- Space defined by lens, zonule fibers, retina
- Filled with gelatinous vitreous humor (water, glycosaminoglycans)


Development of eye

Interaction of ectoderm and mesoderm (neural tube)
- Diencephalon--> optic vesicles (grow out from brain)
- Optic vesicles fold in to form optic cups

Optic cups:
- Inner layer= retina
- Outer layer= retinal pigment epithelium

Optic vesicles--> induce lens--> induce cornea from ectoderm

Mesoderm: forms vascular, muscular, connective tissues


Organization of Retina

1. Retinal pigment epithelium
2. Rod/Cone photoreceptor outer segments
3. Outer limiting membrane
4. Outer nuclear layer (photoreceptor cell bodies)
5. Outer plexiform layer
6. Inner nuclear layer
7. Inner plexiform layer
8. Ganglion cell layer
9. Nerve fiber layer
10. Internal limiting membrane

Basic layers:
1. Retinal pigment epithelium
2. Photoreceptors= phototransduction (light to neural activity)
3. Interneurons= process neural signals
4. Ganglion cells

Specializations of retinal layer:
1. Optic disk/papilla (optic nerve, blind spot)
- When looking at something, blind spot in one eye compensated by other side/brain

2. Fovea= back of retina in line with visual axis
- No blood vessels (gets nutrition from surrounding area)
- All cones- least amount of refraction through retina
- Cells spread to form pit--> maximal visual acuity

3. Ora serrata:
- Anteriormost border of neural retina
- 10 layers collapse to 2= pigmented epithelium (no rods, cones, ganglion)


Organization of anterior eye (choroidal layer, corneo-scleral layers)

Iris= regulates light entering eye
- changes size of pupil
- via sympathetic innervation of dilatory pupillae
- Parasympathetic constrictor pupillae

Cilliary body= regulates fine focus
- Adjusts shape of lens
- Parasympathetic ciliary muscle

Ciliary process= aqueous humor production

Zonule fibers
- Fine ligaments connecting ciliary body to lens


Anterior Chamber angle of eye

Limbus= point of transition from sclera to cornea

Sclera= Opaque, dense connective tissue covering posterior 5/6 of eye
- Insertion site of extraocular muscles

Cornea= Transparent avascular cover over anterior 1/6 of eye
- Primary refractive element of eye

Canal of Schlemm= largest channel of trabecular meshwork
- Drains aqueous humor
- Blockage--> glaucoma


Organization of Iris

Anteriormost specialization of retinal layer
- Regulates amount of light entering eye by changing size of pupil

Sympathetically innervated dilator pupillae
- Myoepithelial cells derived from Retinal Pigmented Epithelial layer (RPE)

Parasympathetically innervated constrictor pupillae smooth muscle

Highly vascular loose connective tissue and pigmented cells

Inner surface lined by pigment cells (neural retinal layer)


Organization of cornea

Five layers:
1. Stratified squamous non-keratinized corneal epithelium
2. Bowman's (basement) membrane
3. Regular connective tissue= substantia propria (stromal layer)
4. Descemet's (basement) membrane
5. Simple squamous corneal endothelium


Organization of lens

Biconvex transparent avascular tissue
- Provides fine focus for visual image
- Changes shaped via ciliary muscle

Outer capsule= connective tissue

Anterior epithelial cells= differentiate into elongated fiber cells

Opacities= cataracts


Organization of eyelid

Protects exposed surface of eye
- Outer surface= thin skin
- Inner surface= conjunctiva (stratified columnar epithelium with goblet cells)

- Tarsal plate (fibroelastic connective tissue)
- Orbicularis muscle
- Large sebaceous Meibomium glands
- Small sebaceous Zeis glands
- Moll sweat glands


Lacrimal glands

Secrete tears
- Tubulo-alveolar serous glands
- Large lumens, few ducts
- Looks similar to pancreas (no Islets of Langerhans)


Diabetic retinopathy: mechanisms of hyperglycemic damage

Diabetic retinopathy= microvascular disease due to chronic hyperglycemia

• Thickened basement membranes:
- Hyperglycemia--> protein synthesis (glycoproteins, part of BM)--> increased thickness--> hindered diffusion

• Sorbitol toxicity (Aldose reductase)
- Converts glucose--> fructose and sorbitol
- Enter cells, do not leave well--> osmotic effects
- Inhibit aldose reductase--> decrease cataracts, pericyte loss, nephropathy, neuropathy

• Glycosylation (HbA1c)
- Higher affinitiy for O2 than normal hemoglobin--> less O2 released to tissues

• Erythrocyte abnormalities
- Glycosylation of the red blood cell membranes makes them more rigid
- Increased plasminogen and macroglobulins impede RBC rouleaux formation and cause clumping
- Both of these mechanisms impede blood flow through capillaries

• Platelet abnormalities
- Diabetic platelets are “stickier”
- Diabetic platelets aggregate faster in response to thrombin, ADP, epinephrine, and collagen

• Circulatory abnormalities
- Hyperglycemia impairs autoregulation of blood flow
- So, for example, in response to hypoxia, blood flow is not increased enough


Earliest findings of capillary damage

1. Thickened basement membranes

2. Pericyte dropout
- Pericytes are contractile cells which regulate flow through capillaries

3. Microaneurysms
- Degenerate and leak
- See hard exudates, macular edema


Non-proliferative Diabetic Retinopathy (NPDR)

Confined within retina:
• Dot and blot hemorrhages
• Microaneurysms
• Cotton wool spots
• Venous beading (sausage veins)
• Hard exudates
• Macular edema

Grade from Mild to Severe:
- Mild= small microaneurysms; leak dye
- Moderate= more dot and blot hemorrhages
- Moderately severe= see marked hard exudates, soft exudates (cotton wool spots)
- Severe= increased hemorrhages, dilated/beaded veins, intraretinal microvascular abnormalities

Macular ischemia= loss of capillaries supplying fovea
- Cause of vision loss in NPDR


Proliferative Diabetic Retinopathy

Worse prognosis
• With time, increasing capillary nonperfusion causes retinal hypoxia.
• In some cases, growth factors like VEGF stimulate the growth of new vessels (PDR)
• Neovascularization of the disc (NVD)
• Neovascularization elsewhere (NVE)

The NEW fragile vessels tend to bleed.
• Fibrous tissue grows along the vessels.
• When the fibrovascular tissue and vitreous contract, the vessels bleed.
• Further contraction can also cause retinal detachment and blindness.

Vitreous traction
- Abnormal blood vessels tether gel and pull on vitreous--> retinal detachment


Symptoms of macular edema

• Blurred vision
• Distortion
• Difficulty with night vision or reading
• Diabetic macular edema is the leading cause of vision loss in diabetic patients, decreased vision in working Americans


Predictors for severity of diabetic retinopathy

TTractional Retinal Detachment
Risk Factors: Severity depends on
• Duration of the disease
• Age of onset
• Glycemic control (A1C levels > glucose level)
• Blood pressure control
• Serum lipid levels

Risk factors:
• At onset: No retinopathy
• After 5 years: 25%
• After 10 years: 60%
• After 15 years: over 80% with some DR
over 25% with PDR
** After 25 years: nearly all diabetics have some D.R.

• Severe retinopathy in children is rare.
• As a general rule, the years one has diabetes before puberty do not count as regards the development of retinopathy.
• So, assuming puberty at 12, any child whether he got diabetes at 1, 2, 3, or 8, would not be expected to develop retinopathy until age 17.


Prevention of diabetic retinopathy

• Control of glucose
- Glycemic control
- HbA1c < 7.1 delayed onset of retinopathy, nephropathy, neuropathy
• Control of blood pressure
• Control of blood lipids
• Control of sodium intake


Focal Laser treatment

Used for diabetic retinopathy
- Beam stops some of vascular growth
- Leaves small focal visual defects
- 3 years post-treatment, risk of doubled visual angle (20/40 to 20/80) decreased by 50%


Other treatments for diabetic non-proliferative retinopathy

1. Intravitreal corticosteroids
• Injections (triamcinolone)
• Implants (fluocinolone, dexamethasone + PLGA intravitreal delivery for 35 days)
- Complications: increased IOP, endopthalmitis (infection), cataracts

2. Other pharmacologic treatments
• Anti-VEGF drugs
- revolutionized diabetic retinopathy
- VEGF activity correlates with degree of diabetic retinopathy
- Drugs: Macugen, Avastin (antibody to VEGF), Lucentis (fragment of Ab), Eylea (fusion protein)
• Protein Kinase C Inhibitors

3. Parsplanavitrectomy (remove vitreous humor)


Treatment of Proliferative diabetic retinopathy

1. Panretinal laser photocoagulation
- Apply laser to entire midperipheral fundus
- Complications
• Slight decrease in vision
• Slight decrease in night vision
• Slight decrease in peripheral vision

2. Vitrectomy surgery
- Used in patients with non-clearing vitreous hemorrhage
- Tractional retinal detachment
- Complications: major procedure, eyes/patients have poor risks, costly


Tractional Retinal Detachment

Cut adhesions between vitreous and retina
- Adhesions cause vitreous to pull on retina--> retinal detachment
- Correct tractional retinal detachment
- Remove scarred tissue overlying retina (from previous laser surgeries)


Causes of Red Eye

1. Conjunctivitis
- Discharge

2. Keratitis (inflammation of cornea)
- may have discharge
- Painful
- Decreased vision
- pupil size may change

3. Iritis
- Painful
- may have Decreased vision
- Unequal pupil

4. Acute angle closure glaucoma
- Painful
- Decreased vision
- Dilated pupil

- Pterygium
- Episcleritis
- Scleritis
- Dacryocystitis



Chief complaint: foreign body sensation

1. Viral:
- watery discharge
- tender palpable preauricular node
- recent URI
- Highly contagious
- Spread by eye-hand-eye contact
- Hand washing is of critical importance
- Treatment: Cool compresses and lubricating drops for most cases

2. Allergic:
- itching
- Stringy, white discharge
- See bumps on underside eyelid
- Associated with atopic disease
- Treatment: cool compress, topical antihistamine, NSAID, mast cell stabilizer, systemic antihistamines (only if NOT dry eye)

3. Bacterial:
- purulent discharge
Gram +
- Staph aureus and epidermidis
- Strep pneumoniae
- Strep Groups A & B
- Corynebacterium diptheriae
Gram -
- Hemophilus influenza
- Pseudomonas aeruginosa
- Neisseria gonorrhoeae and meningitidis
Culture with conjunctival swab
- topical antibiotic drop (polymyxin/trimethorpim, moxifloxacin, gatifloxacin, besifloxacin, azithromycin)
- Topical antibiotic drop (erythromycin, bacitracin)
** in hyperacute conjunctivitis, need to rule out GC (gonococcal conjunctivitis) by gram stain


Red eye in infants

- Ophthalmia neonatorum (neonatal conjunctivitis)
- Dacryocystitis
- Congenital glaucoma

1. Chemical - silver nitrate: 10% incidence with silver nitrate
- Onset within 2-4 hours
- Duration 24-48 hours
- Treatment: Lubrication and close follow-up
2. Chlamydia
3. Gonococcus
4. Others (e.g. staph, strep, pseudomonas)

- Erythromycin ophthalmic ointment
- Azithromycin gel drops


Chronic conjunctivitis

Toxic (medications)
Molluscum contagiosum of the eyelids
Allergic (seasonal or vernal/atopic)


Chlamydia conjunctivitis

Neonates and sexually active adults
- Can cause systemic disease in neonates (e.g. otitis, pneumonitis)
- Lasts weeks to months without treatment in adults

- Systemic tetracyclines, azithromycin, erythromycin for 3-6 weeks



Inflammation of the eyelid margin
- Crusting of the eyelashes, typically worse in the morning
- Associated with dry eyes
- Clogged Meibomium glands (zits)

- Warm compresses
- Eyelid scrubs, antibiotic ointment
- Occasionally systemic tetracyclines, azithromycin


Topical fluorescein dye

- Vegetable dye picked up by areas absent of epithelium
- Appears green with cobalt blue light
- Extremely useful in diagnosing corneal abrasions, lacerations, foreign bodies, etc.

** NOTE: Be careful as serious corneal injuries and infections can also stain with fluorescein


Corneal problems

- Foreign bodies
- Chemical burns
Contact lens complications
Bacterial ulcers
Herpes simplex virus infections
Other infections
- (e.g. fungus, acanthamoeba, herpes zoster)


Contacts causing Red Eye

GPC (giant papillary conjunctivitis)

Tight contact lens syndrome

Toxic/allergic reaction to chemicals in contact lens solutions

Bacterial corneal ulcers (pseudomonas especially)

Acanthamoeba keratitis (uncommon parasitic corneal infection)


Treatment of corneal ulcers

Mild to moderate, peripheral
- Topical fluoroquinolones
1. Cipro= pseudomonas, staph, strep
2. Ofloxacin= broad spectrum
3. Levoflox= broad spectrum
4. Moxi, gati, besi= 4th generation
- Good gram neg coverage
- Improved gram pos coverage
- better penetration

Moderate to severe, central
- Topical fortified antibiotics:
1. Tobramycin (15 mg/ml) q 30-60 minutes ATC alternating with
2. Cefazolin (50 mg/ml) q 60 minutes ATC


Herpes simplex keratitis

1. Active infection:
- Classic tree branch pattern epithelial defect=dendrite
- Tx: topical and/or oral antivirals
*** Made WORSE by steroids in active infection***

2. Inflammation:
- Can cause corneal edema and inflammation inside the eye (iritis)
- Tx: topical steroids w/ anti-viral coverage



Signs/symptoms: circumcorneal injection, photophobia

Secondary to blunt trauma, keratitis

Associated with systemic diseases (e.g. sarcoidosis, connective tissue disorders)



Referral not necessary for following:

Conjunctivitis improving over 2-4 days
Tx: cool compresses and tears

Tx: warm compresses

Subconjunctival hemorrhage (nontraumatic)
Tx: none


Steroid complications in eye

Glaucoma (in susceptible patients)

Cataract (dose related)

Enhances most active infections, especially:
- Herpes simplex infections
- Fungal infections
- Acanthamoeba infections


Concerning signs/symptoms in red eye

Danger symptoms:
- Decreased vision
- Pain
- Photophobia

Danger signs:
- Corneal fluorescein staining
- Corneal edema
- Circumcorneal injection
- Abnormal pupil size or reaction
- Abnormal eye pressure

Urgent conditions (referral to optho):
- Corneal infection
- Iritis
- Angle closure glaucoma
- Orbital cellulitis
- Trauma: Hyphema (blood in anterior chamber), Laceration


Vascular supply to eye

Choroidal artery= back of retina
Retinal artery, vein


Retinal vascular disease

- Artery Occlusions
- Vein Occlusions
- Hypertension/ Arterial Sclerosis
- Amaurosis Fugax
- Ocular Ischemic Syndrome
- Diabetes Mellitus
- Sickle Cell Disease


Types of retinal hemorrhages

Streak/flame hemorrhages
- Superficial
- Nerve fiber layer- gives streak configuration
- More with arterial disease (hypertension)

Dot and blot hemorrhages
- Deeper retina
- Outer plexiform layer- gives round configuration (“blot” larger than “dot”)
- More with venous disease (retinal vein obstruction)


Cotton Wool spots

- Small foci of fluffy retinal whitening
- Located in retinal nerve fiber layer
- Occur secondary to blockage of terminal retinal arterioles

Histopathology: Regions of axoplasmic damming in the nerve fiber layer


Hard exudates

- Discrete yellow deposits in the retina
- Located in outer plexiform layer
- Occur secondary to chronic leakage of lipids from incompetent retinal vessels (or subretinal neovascularization)


Branch retinal artery occlusions

= Blockage of retinal artery
Edematous opacification of the retina :
- Within hours/days
- In the distribution of the affected vessel
- Embolus may be visible

Emboli= #1 cause
- Cardiac
- Irregular heart rate
- Cardiac valves
- Carotid plaques
- Hypercoagulability
- High Blood Pressure

Types of emboli:
1. Cholesterol “Hollenhorst plaques”
- Arise from carotid
2. Platelet-fibrin
- Associated with arteriosclerosis
3. Calcific
- Diseased cardiac valves


Central Retinal Artery Occlusion

= Sudden, painless visual loss

Retinal appearance:
- Opaque and edematous
- Cherry-red spot”= unobstructed choroidal vasculature (outer retina) in tact, retinal vasculature gone
- Visible intact choroidal vasculature beneath the foveola

- Atherosclerosis (Majority)
- Arterial spasm (e.g. migraine)
- Dissecting aneurysm
- GIANT CELL ARTERITIS= 1% of cases (rare, but can become bilateral quickly)

- No good therapy exists
- If within 24 hrs
- Anterior chamber paracentesis (withdraw fluid from front of eye)
- Ocular massage (pressing on eye dilates arterioles)
- Lower intraocular pressure
- Carbogen (5% CO2, 95% O2)

Complications (more common in central occlusions):
- Iris neovascularization: Due to ischemic retina; Usually 3-4 weeks later
- Laser treatment required


Branch retinal vein occlusion

Within one sector or retina; occur where vein and retina cross frequently:
- Superficial hemorrhages
- Retinal edema
- Cotton-wool spots -
- Dilated and tortuous vein
- Corresponding artery narrowed and sheathed

Risk factors:
- Age 60-69 most common
- Hypertension
- Cardiovascular disease
- Increased BMI at age 20
- Glaucoma
- Hypercoaguable states (esp in younger patients)

Causes of visual loss
- Macular hemorrhage
- Macular edema
- Capillary occlusion (macular ischemia)

1. Macular edema
- Laser
- Intravitreal triamcinolone or antiVEGF agent
2. Neovascularization
- PRP to ischemic area


Central Retinal Vein Occlusion

= Dilated and tortuous retinal veins all 4
- Optic disc swelling
- Intra-retinal hemorrhages
- Macular edema
- Cotton-wool spots

- Throbosis of central retinal vein at or posterior to the lamina cribrosa

Risk factors:
- Age (90% > 50 y.o.)
- Hypertension
- Diabetes
- Glaucoma
- Hypercoaguable states (especially in young patients)

- Family medical doctor to manage
- Hypertension
- Diabetes
- Elevated cholesterol

- Neovascularization: Laser (panretinal photocoagulation- permanent, shirinks vessels)--> avoid glaucoma by catching before vasculature moves into angle
- Macular edema: Intravitreal triamcinolone; Anti VEGF agents (temporary)


Ocular effects of systemic arterial HTN

Grade I (chronic)
- Retinal arterial narrowing
- Straightened retinal arteries

Grade II (chronic)
- Retinal arterial narrowing
- Straightened retinal arteries
- Arteriovenous nicking at AV crossings (vein underneath artery--> squished)

Grade III (acute)
- Retinal hemorrhages
- Cotton-wool spots
- Hard exudates
- Diastolic BP > 110-115 mmHg

Grade IV (malignant hypertension)
- More severe grade III changes plus:
- Optic disc swelling (elevated margins)
- Diastolic BP > 130 mmHg
- Systemic prognosis is poor

- Grade I changes from aging alone
- Fundus findings not helpful in managing htn unless Grade III or IV
- Only Grades III and IV adversely affect the vision; Rx: treat the hypertension
- For Grade III and IV changes- move on it!


Amaurosis Fugax

“Fleeting blindness”
- Unilateral, transient (seconds to minutes) loss of vision
- Usually fibrin-platelet thrombi from the carotids
- Incidence of subsequent stroke is 4% per year

Tests: Trans-carotid US, CT


Ocular Ischemic Syndrome

>90% ipsilateral carotid artery obstruction
- Relatively rare clinical entity

- None
- Visual loss over weeks to months
- Periorbital aching pain

- Rubeosis iridis (iris neovascularization)
- Dilated but not tortuous retinal veins
- Mid-peripheral retinal hemorrhages

Prognosis: Poor
- 40% five year mortality
- Stroke and cardiac events

- Laser for rubeosis
- Carotid endarterectomy/stent

Resembles central artery occlusion, but arteries straight not tortuous
* High risk for stroke, other ischemic events


Sickle cell retinopathy

Clinical features- Spectrum like diabetes

- Salmon patch- acute intraretinal hemorrhage
- Black Sunburst- subretinal pigment clump

- Sea fan- peripheral retinal neovascularization
- Vitreous hemorrhage
- Traction retinal detachment

Causes (in descending order):
- Hgb SC
- Hgb Sthal
- Hgb SS
- Hgb AS (trait)

- Laser therapy for proliferative sickle disease (promotes regression)


Retinopathy of prematurity

- Smaller the baby, greater the chance
- Significant in 75% of babies Peripheral retinal avascular zone
→ Ischemia → vascular growth factors
→ Peripheral retinal neovascularization
→ Retinal detachment or dragging (fibrosis pulls on lens--> tractional retinal detachment (--> blindness)

- Screening exams in NICU
- Babies born <20%


Optic neuropathy: signs

+/- decreased acuity
- RAPD (relative afferent pupillary defect) if asymmetric
- Dyschromatopsia= color vision problems
- Optic nerve may be: swollen, normal, pale


Optic neuritis

- Younger patients (20s-30s)
- Female > Male
- Caucasian, Northern European
- Pain with eye movement (92%)
- Vision loss progressing over 1-2 weeks

- Decreased visual acuity (usually unilateral)
- Decreased color vision
- Relative afferent pupillary defect – RAPD
- Visual field defect: central scotoma (darker in center) or inferior altitudinal
- Normal optic disc (2/3); Mild edema (1/3)

- Don't need MRI to diagnose optic neuritis
- Brain MRI used to determine MS risk, tx
- Look for enhancement of optic nerve, white matter lesions (Dawson's fingers- perpendicular to ventricles)
- 38% 10 year risk of developing MS
- 56% 10-year risk with 1+ lesions, 22% if no lesions

Treatment: IV steroids for:
- faster visual recovery
- delays onset of another demyelinating events
- oral steroids associated with increased recurrence rates (IV ONLY!)
- IFN beta-1a if 2+ white matter lesions


Anterior ischemic optic neuropathy:

Optic nerve affected close enough to globe--> disc swelling (hence anterior)
- Common features: acute vision loss, disc edema

- Younger age (60s, 70s)
- Vasculopathic risk factors
- No warning symptoms
- No treatment

- Sudden vision loss
- Often upon awakening
- Stable from onset
- May have mild pain
- No prodrome

Risk factors:
- DM
- Elevated cholesterol
- Smoking
- Sleep apnea
- ED drugs

- Acute= swollen nerve
- Hemorrhages, dilated capillaries
- Small crowded disc in contralateral eye
- Inferior altitudinal defect most common

Treatment: ID and manage risk factors (prevent bilateral defects)
- Blood pressure: Blood pressure meds in AM if possible
- Lipid panel
- Hemoglobin A1c
- Smoking Cessation
- ED drugs
- Sleep study (high association with sleep apnea)

- Vision loss remains ~ stable
- Rare to recur in the same eye (death causes decompression)
- About 15 % chance of occurrence in 2nd eye over 5 years


Anterior ischemic optic neuropathy:
Giant cell arteritis (arteritic)

Optic nerve affected close enough to globe--> disc swelling (hence anterior)
- Common features: acute vision loss, disc edema

- Older onset (>70)
- Caucasians
- Vasculitis of med/large vessels
- Bilateral (20 – 60%)
- If unilateral; second eye involvement often within days without treatment (75%)
- Abnl ESR, CRP, CBC
- Other symptoms
- Treated with steroids
** Prevent catastrophic vision loss!
** Protect other eye!

- Vision loss
- Transient
- Constant
- Double vision
- Premonitory symptoms
- RED FLAGS: Episodes of transient vision loss followed by constant loss; Purple or blue vision

Systemic symptoms:
- Jaw claudication
- Scalp tenderness
- Headache
- Temporal tenderness (prominent temporal arteries)
- Weight loss
- Muscle aches
- Fever

- Relative afferent pupillary defect
- Dyschromatopsia (color loss)
- Visual field defects
- Normal appearing or Swollen nerve; “Chalky White”

- ESR, CRP, platelet elevation
- Steroids (IV for acute neuro/visual changes)
- Temporal artery biopsy within 2 weeks
** DON'T wait for biopsy to start steroids


Thyroid-related orbitopathy (TRO)

Thyroid eye disease (TED)= Grave's disease
Thyroid-associated orbitopathy (TAO)
- Mainly occurs in patients with hyperthyroidism (can be in euthyroid, hypothyroid patients)

- Auto-immune
- Infiltration of orbital tissue by inflammatory tissue

Symptoms: Inflammation, edema, fibrosis of orbital contents may result in:
- Eyelid retraction (90% of patients with TRO)
- Proptosis (enlarged tissue)
- Motility Deficits (enlarged muscles)
- Red eye
- Conjunctival injection, chemosis
- Keratopathy
- Optic neuropathy (5% of patients, due to inflammation of tissue)

- Enlarged extra-ocular muscles SPARING TENDON where it inserts into eye
- Crowding at orbital apex

1. Steroids: short term, radioactive iodine
2. Orbital radiation
3. Surgery: done in following order:
- Orbital Decompression (Optic neuropathy: urgent)- move floor down
- Strabismus surgery
- Eyelid surgery (correct eyelid retraction)

** Smoking makes it worse!!


Inflammatory Orbital Pseudotumor

Idiopathic orbital inflammatory syndrome (IOIS)
** Not to be confused with pseudotumor cerebri**

Can involve ANY orbital tissue:
- Muscles
- Lacrimal gland
- Optic nerve
- Sclera

- Protosis (muscle inflammation)
- Pain- scleral involvement
- Double vision (diplopia)- muscles
- Loss of vision- nerve
- Red eye

- Radiology may show enlarged muscles INCLUDING TENDONS (vs TRO)
- Biopsy if atypical
- VERY responsive to steroids


Ocular Myasthenia Gravis

Autoimmune reaction affecting NM junction
- Reduced number of Ach receptors due to auto-antibodies against receptors

- Generalized weakness
- Ocular only: “Ocular Myasthenia Gravis”
- Fatiguable muscular weakness
- Eyelids/extraocular muscles involved in > 90% (double vision, ptosis= variable, fatiguable)

- Ice test (close eyes, apply ice- should open more afterwards)
- Tensilon test (edrophonium chloride)- dangerous
- Acetylcholine Receptor Antibody Testing (negative in up to 50%, esp. in Ocular MG)
- Single Fiber EMG including orbicularis oculi muscle

1. Pyridostigmine (mestinon)
- Inhibits acetylcholinesterase
2. Chest CT to evaluate for thymoma
3. Advise patient to go to ER or call 911 if difficulty:
- Breathing
- Speaking
- Swallowing


Visual development

Neonatal vision:
- At birth, vision is approx. 20/200 (10% adult vision)

Requirements for vision development:
Image must be clearly focused onto the fovea. In order for this to occur there must be:
1. Symmetric refractive error
2. Straight eyes
3. No organic pathology obstructing clear visual axis (cataracts at birth can stop development)

Binocular vision, stereoacuity serve two functions:
1. Stereopsis= depth perception
2. Permanency= maintains eye alignment long term
** more aggressive correction in younger children to try and salvage neurological pathways
- Until age 7, poor vision results if clear image is not focused on fovea of each eye
- The earlier the onset of amblyopia, worse its prognosis



Methods to evaluate:
- Vision
- Stereopsis
- Rotations
- Measurement of deviation in different gaze positions

1. Comitant strabismus:
- Deviation is same regardless of gaze
- No known neuromuscular etiology
- Common in children
2. Incomitant strabismus:
- Size of Deviation varies in different gaze:
- Increases when gaze is in direction of the involved muscle.
- Less common than comitant strabismus
- Common causes include:
* Cranial Nerve palsy
* Thyroid Eye Disease
* Mechanical restriction


Types of strabismus

Esotropia: eyes turn inward
Exotropia: eyes turn outward
Hypertropia: one eye higher than the other
Hypotropia: one eye lower than the other


Comitant strabismus: Congenital Esotropia

- Seen within first few months of life
- Mechanism unknown
- Amblyopia common
- Treatment is usually surgical
- Commonly need further surgery or glasses before age 5


Comitant Strabismus: Accomodative Esotropia

- Develops age 1 -4
- Intermittent at first, increases over time
- Amblyopia common

- Occurs in hyperopic/farsighted eyes
- Accommodation is mechanism used by all to see clearly
- Accommodation is linked to convergence
- Excess accommodation leads to excess convergence, or esotropia

Treatment is glasses
- These eliminate need to accommodate and therefore, lessen excess convergence
- Children wear glasses happily, as crossing is uncomfortable, until at least age 10
- 70% of children outgrow glasses as eyes enlarge (too short in early life--> farsighted)
- 15% of patients require surgery in addition to glasses


Comitant Strabismus: Sensory esotropia

- Occurs in eye with poor vision (congenital)
- Surgery straightens eye, but will not affect vision, will be needed often to straighten eye
- Surgery will likely need to be repeated in 10-15 years


Idiopathic exotropia

Begins intermittently; often increases in frequency and duration.
- Usually worse at distance
- Mechanism unknown
- Amblyopia common (treat ambylopia, see if orientation corrects)
- Treatment is often strabismus surgery


Sensory exotropia

Occurs in an eye with poor vision
- Surgery is done to straighten the eye, but will not improve visual acuity
- Surgery will likely be necessary again within 10 -15 years


Incomitant strabismus: CN3 palsy

Measurements of vision different with different gazes

- Levator muscle, resulting in ptosis
- Pupillary fibers, resulting in dilation of pupil
- Four of six extraocular muscles knocked out, leaving eye “down and out”.

- Congenital
- Trauma
- Aneurysm

Treatment very difficult with only two working muscles, but some patients do well with surgery


Incomitant strabismus: CN4 palsy

Measurements of vision different with different gazes

- Involves the superior oblique muscle
- Mechanism typically: congenital, trauma
- Patient presents with VERTICAL diplopia, worse in downgaze opposite the involved muscle
- Often use a HEAD TILT to manage diplopia

- Glasses with prism if degree of diplopia small
- Surgery if degree of diplopia large (inferior oblique weakened so it doesn't overpower denervated Superior oblique)
- Patients do very well with appropriate option


Incomitant strabismus: CN6 palsy

Involves the lateral rectus muscle

- Trauma
- Tumor
- Inflammation (viral infection)
- Vascular

- Patient presents with HORIZONTAL diplopia, worse in gaze towards the involved muscle
- Patients adopt a FACE TURN to eliminate diplopia

- Prism glasses for small degree of diplopia
- Surgical correction
- Many resolve on their own and do not require treatment


Mechanical limitation of eye movement

Blowout fracture
Orbital mass



Visual issue often occurring with strabismus

- Refractive (49%)
- Strabismus( 49%)
- Ocular Pathology (2%)
1. Cataract
2. Glaucoma
3. Corneal anomaly

- Eliminate cause: correct strabismus, provide corrective glasses, remove cataract
- Force patient to use weaker eye with patch, Atropine dilating drops
** Rarely successful after age 8



Must use a sticky, bandaid like patch

Amount of patching needed to improve vision is related to:
- Degree of initial visual impairment
- Age at time amblyopia first discovered

** Once vision improved, must patch 1 hour a day until age 8 - 9


Nasolacrimal system

80% of drop in cul-de-sac drains into the lacrimal system

Punctal occlusion decreases the amount of drug entering the nasolacrimal system by 65%
- Reduce systemic toxicity, tasting the drops

Systemic absorption occurs primarily through the nasolacrimal system (highly vascularized nasopharyngeal mucosa with no first-pass effect through GI tract and liver).


Tear Washout

Washout effect of spontaneous tear flow causes disappearance of a drop from the cul-de-sac within 5 minutes

So, best time interval between drops is 5 minutes
- Okay to redose immediately (multiple drops can't fit into cul de sac)
- Chilled drops- know where it landed


Central vision

Measure of macular function
- Measures two disc diameters from optic nerve to temple
- Measured with Snellen chart



Elements of refractive errors:



Lens of sufficient convex power to bring parallel light rays to focus at 1 meter

Diopter= 1/focal distance
ex: 2 diopter lens= brings focus in at 1/2 meter (50 cm)



Parallel light rays focused on retina in unaided eye
Eye is 60 diopter= 1/60 meter long
- Cornea= 40 diopters
- Lens= 20 diopters

* Ametropia= parallel light rays NOT focused on retina



Parallel light rays focused in FRONT of fovea
- Retina presented with diverging rays

- Increased corneal curvature
- Longer axial length
- Increased refractive index of lens due to nuclear sclerosis

- Blurred distance vision
- Squinting (pinhole effect): narrowing aperture to decrease refraction
- Holding reading close

- Divergent (concave) lens
Ex: +64.00 Diopter eye corrected by -4.00 lens



Parallel light rays brought into focus at point BEHIND retina

- Shorter axial length of globe
- Decreased refractive power of cornea, lens

- Corrected by convex lens power
- Eye presented with converging rays
Ex: + 56.00 diopter eye corrected by +4.00 lens



Lack of a point focus
- Refractive surfaces are not sperical- have 2 radii
- 2 focal points can't be brought together as eye is not sperical (egg-shaped)

- Combination of spherical and cylindrical lens power



Accomodative ability of eye cannot bring objects into focus on retina
- With near objects, eye is presented with diverging rays instead of parallel rays

Common symptoms:
- Can't read phone book
- Can't thread needle
- Stock fractions difficult
- Push reading away

- Bifocals
- Full reading lens: blurs distance, easy adjustment
- Half glasses: looks funny, can see in distance
- Mono vision contact
- Bifocal: good distance and near, harder adjustment



Ability of lens to change shape, become more convex
- Increases refractive power



Absence of lens
- Eye is now short 20 diopters short of refracting power

- Contact lens (old person can't put in)
- Thick glasses (hard to walk in these)
- Lens implant (issue with children, won't grow with eye)


Refractive surgery

Refractive surgery principles:
- Myopia= flatten apical cornea
- Hyperopia= steepen apical cornea
- Astigmatism= segment selective flattening

Radial keratotomy:
Removing some of keratin layer of eye--> improve vision
- Flattening determined by number/depth of incisions
- Now used as "touch up" procedure
- Weakens cornea
- Long term change in refraction

Photorefractive keratotomy:
- Excimer laser ablation of corneal stroma
- Apical for myopia
- Peripheral for hyperopia
- Pros: easy to perform, best in myopia up to -7.00
- Cons: post-laser pain, longer recovery, cornea haze

Lasik= Laser in-situ keratomileusis
- Hinged corneal flap created
- Laser ablation of stroma
- Flap replaced
- No sutures used

Intraocular lens implants:
- Remove clear lens for improved lens


Legal blindness

Best corrected vision of 20/200 or less in the BETTER eye
- Visual field < 20 degrees

Worldwide causes:
- Cataract
- Glaucoma
- Trachoma (Chlamydia)
- Onchocerciasis (River Blindness)

US causes:
- Macular Degeneration
- Glaucoma
- Cataract
- Diabetic Retinopathy


Age-related Macular Degeneration (ARMD)

Most common cause of blindness
1. Dry (non-neovascular)
2. Wet (neovascular)

Risk factors:
- Age
- Family History
- Hypertension
- Increased Cholesterol
- Smoking

- The outer retina is supplied by the choriocapillaris
- An intact retinal pigment epithelial (RPE) layer is crucial to the function of the overlying cones and rods
- Damage occurs between Bruch's Membrane and Choriocapillaris--> breaks in RPE

- Deposition of eosinophilic material
- Thickening and fragmentation of Bruch’s membrane
- Degeneration of the RPE and loss of overlying photoreceptors


ARMD: dry type

Clinical features:
- Drusen Formation (Yellowish-White Bodies)
- Usually cluster in posterior pole (central vision affected- very noticeable)
- RPE Atrophy and Pigment Clumping
- Slowly Progressive
- Gradual Decrease in Vision
- Peripheral Field Remains Intact
- May be Devastating Psychologically

- Vitamin combination with Zinc and Lutein slows progression approximately 25%.


ARMD: wet type

Usually preceded by dry type
- New blood vessels from choriocapillaris membrane--> Bruch's membrane--> Retina
- Form choroidal neovascular membrane = CNVM
- New vessels bleed

Clinical features:
- Sudden Decrease in Vision, Distortion
- Hemorrhage, Edema, Exudates in Macular Area
- Drusen, RPE Changes
- Recurrences

Measured with Amsler Grid: can map retinal defects based on where lines are distorted (top, bottom, L, R)

- Laser photocoagulation of the CNVM (could worsen vision)
- Photodynamic Therapy (PDT)= Chemical injection followed by laser
- Inhibition of VEGF- YAY!
- Other



An optic neuropathy in which intraocular pressure which is too high for a given optic nerve causes damage to the nerve and visual field loss

Normal physiology:
- The anterior portion of the eye is filled with Aqueous
- Secreted by the Ciliary Body
- Circulates through the Anterior Chamber
- Drained from the eye primarily through (Trabecular Meshwork)

Open angle: most common, asymptomatic
Closed angle: symptomatic


Open angle glaucoma

Most common, asymptomatic
- Trabecular meshwork not draining
- Chronic, progressive over years
- Good central vision until late in disease (will just move head to compensate for visual field losses)
- Unknown etiology

Risk factors=
- Age
- Family history
- Race (AAs)
- Steroid use/response

- “Elevated” IOP?
- Optic disc appearance= cupping (loss of neuroretinal rim)- cup should be < 1/2 size of nerve: glaucoma--> increased cup
- Visual field change= gradual

- Medical (Prostaglandin inhibitors, beta-blockers, CA-Inhibitors
- Laser (to the Trabecular meshwork)
- Surgical: creation of alternate drainage channels (Trabeculectomy + "trap door"- increased risk for eye infection for remainder of life, Tube Shunt)


Closed angle glaucoma

Less common than open angle, Symptomatic
- Fluid can't access trabecular meshwork
- Phaecomorphic: Lens swells (cataract) pushing iris forward--> fluid can't move from behind lens toward meshwork

- The area between the iris and cornea suddenly closes, blocking drainage
- Short (hyperopic) “crowded” eye is a risk factor

- Red painful eye
- Cloudy cornea
- Fixed, mid-dilated pupil
- Pain, possible nausea
- Decreased vision (hazy cornea)
- Elevated IOP (push on eyes while closed- attack causes eye to become harder)
- Conjunctival injection
- Corneal edema

- Reduce IOP with topical agents
- Systemic osmotic agents
- Laser iridotomy in EACH Eye (bring pressure down to protect vascular inflow- vs nerve damage in chronic open angle glaucoma)= making a small hole in iris to allow aqueous humor to access trabecular meshwork



Reversible Opacification of lens

Risk factors:
- Age, Age, Age
- Heredity
- Trauma
- Steroid Use
- Certain Diseases: Diabetes, Retinitis Pigmentosa

- Cortical
- Nuclear Sclerosis= vision, colors affected
- Posterior Subcapsular= reading vision affected (younger pts, steroid users)

Treatment: Surgical
- Indication: When the decreased vision interferes significantly with daily function or quality of life
- Most common procedure
- Small incision
- Phacoemulsification (Ultrasound)
- Foldable lens implant

Visual correction after surgery: Lens accounts for a significant amount of refractive power (focus). Replaced by:
- Intraocular lens implant
- Contact lens
- Thick glasses (convex)

** High Success Rate
- Reasons for Failure:
Other Conditions
Infection, Hemorrhage
Corneal Decompensation


Causes of Refractive changes

Surface disease: dry eyes, epithelial defects

Cornea: dysfunction/ inflammation/ edema

- Inflammation- flare and cells= hypopion
- Blood= hyphema

- Cataract
- Lens dislocation (zonule fibers knocked out of place)

- Vitritis
- Hemorrhage
- Intravitreal foreign body


Circulatory emergencies in the eye

Arterial occlusions:
- Longstanding= vasculopathy
- Embolic: find origin

Venous occlusions:
- Manage systemic condition (HTN)


Retinal detachment

Neuro-sensory part of eye detaches from vasculature
- "Curtain dropping down"
- Must correct ASAP to prevent ischemia, central vision loss


Lid lacerations

Most serious injuries occur at lid margin
- Must call in Plastic surgery
- Ensure properly repaired to prevent abraisions, loss of tear duct function


Corneal abraision

Rule out Intra-ocular foreign body
Topical anesthesia helps diagnosis
Warn of continued pain
Topical antibiotic solution/ointent
- See next day if abrasion large/central (can recur as it heals and adheres to lid

NEVER prescribe ongoing topical anesthetic- eats away at cornea


Blunt trauma to the eye

Hyphema (blood in anterior chamber)
Traumatic iritis
Dislocated lens
Ruptured globe
Orbital fracture


Blowout fracture

Vertical diplopia= Inferior oblique/rectus blowout

Subcutaneous air= ethmoid bone fracture
- Precautions for blowing nose

Decreased sensation in infra-orbital nerve distribution= cheek (maxilla) fracture

** Shield eye with cup, don't compress to protect it



- can cause pupillary distortion (internal structure damage, ruptured globe)
- poor vision
- shield eye
- look for other blood problems (sickle cell)

- Topical steroids (reduce inflammation), but monitor IOP
- Cycloplegia (comfort, exam)
- Bed rest, upright to help RBCs settle (clot)


Trauma to posterior segment of eye

Retinal edema--> hemorrhage--> macular edema

Choroidal rupture
Retinal tear, detachment
Traumatic optic neuropathy
Avulsion optic nerve


Chemical injury to eye

Alkali damage--> whitened cornea due to vascular loss--> necrosis


Child abuse: head trauma

Up to 1/3 of children with head trauma die from injuries

Survivors often suffer permanent impairment:
- Quadriparesis
- Severe developmental delays
- Learning disability
- Motor disturbances

Children who survive may have:
- partial or total blindness
- hearing loss
- seizures
- developmental delays
- impaired intellect
- speech and learning difficulties
- problems with memory and attention
- severe mental retardation
- paralysis (some particularly traumatic episodes leave children in a coma)


Eye in child abuse

Extent and type of hemorrhage associated with severity of neurologic injury, mortality

Circular retinal folds, retinal detachment associated with severity of CNS injury and mortality

Visual impairment in up to 1/3 of children
- Most commonly from cortical visual loss or optic atrophy


Clinical findings in shaken baby syndrome

History provided often incompatible with developmental stage of infant
- Unwitnessed trauma claimed
- Different versions offered at different times or by different care-givers

Perpetrators: most commonly dad, then live-in boyfriends, babysitter, mother


Signs and Symptoms of Shaken Baby

Violent cases:
- unconscious, suffering seizures, or in shock

Less severe cases
- Lethargy, irritability, vomiting
- poor sucking or swallowing, appetite
- lack of smiling or vocalizing
- Rigidity, difficulty breathing
- altered consciousness, inability to lift head
- unequal pupil size, inability to focus eyes or track movement

- Retinal hemorrhages
- Skull fractures
- Swelling of the brain
- Subdural hematomas
- Rib and long bone fractures
- Bruises around the head, neck, or chest

Perpetrator grabbing child:
- by a limb, signs may include hemorrhagic stripping the long bone periosteum and metaphyseal chip fractures
- by the chest, multiple posterior-lateral rib fractures may occur
- Skeletal survey and skin inspection


CT or MRI findings in Child Abuse

Subdural hemorrhage

Subarachnoid hemorrhage
- In particular, posterior inter-hemispheric hemorrhage

Diffuse cerebral edema
- Occlusion and nonperfusion in the distribution of the major cerebral vessels

Less common: parenchymal contusion, hemorrhage, or laceration

Brain injury caused by angular (rotational) acceleration and deceleration of head during shaking
- CSF protects brain in translational inertia
- Impacts act as harmful lubricant in rotational trauma
- Brain lags behind skull during high angular acceleration
- Strain bridging veins passing from brain through subarachnoid and subdural spaces to the dural venous sinuses
- Bridging veins tear leading to SDH

Shearing effects tear axon of brain
- Most damage due to ischemia from shearing


Retinal hemorrrhages

Seen in about 85% of shaken baby/ abusive head trauma victims

1. Subretinal
- Blood vessels seen over the hemorrhage
2, Intraretinal- most common: Blood vessels usually obscured:
- Dot, Blot- round
- Flame- very superficial
3. Preretinal
- Subhyaloid (between retina and vitreous)
4. Vitreous


Retinal folds

- Centered on macula
- May be multiple
- Poor prognosis for neurological recovery, fair prognosis for vision
- Mechanism:
1. Vitreous traction
2. Retinoschisis: SPLITTING!
3. RPE rupture


Unilateral hemorrhages

15% of abused patients with head trauma (rare)

Possibly related to venous obstruction:
- Choking or Throttling
- Asymmetric Force
Look carefully for small hemorrhages on ‘unaffected’ eye


Pathogenesis of Retinal Hemorrhages

Increased ocular pressure due to:
- Increased intracranial pressure
- Increased thoracic pressure
- Strangulation
- Direct tracking of blood from Subdural/Subarachnoid spaces: unlikely
- Mechanical shaking of the globe

- Vaginal delivery or Cesarean
- Child abuse
- Severe accidental injury
- Coagulopathy, Vasculitis, Leukemia
- Severe hypertension, usually with exudates
- AV malformations
- Papilledema (flame shaped, around optic nerve)
- Meningitis
- Metabolic diseases


Terson syndrome

Vitreous and retinal hemorrhage with arterial intracranial bleed
- used incorrectly in abusive head trauma

Completely different mechanisms
- high-pressure arterial bleed
- closed cranial space in adults
- vitreous vs. retinal and preretinal in inflicted trauma
- no circular folds or retinoschisis


Purtscher's retinopathy

- Retinal and preretinal hemorrhages
- Retinal White Patches
- Normal optic disc
- Sudden compression of chest:
1. Transmission of intravascular pressure?
2. Long bone fractures
3. Similar seen with Pancreatitis


Accidental head trauma

"Baby fell off the changing table"

Numerous clinical and post-mortem studies of eyes in patients with severe head injury suggest rate of retinal hemorrhage < 3)
- unilateral/bilateral
- NO retinal folds, retinoschisis
- No associated CNS bleed


Bleeding disorders showing retinal hemorrhage

Usually few, isolated, unilateral
May be large
- not extending to anterior retina
- no circular folds, retinoschisis
- if multiple, suspect trauma instead/in addition to coagulation abnormality

Severe anemia
Hemophilia and factor deficiencies
Glutaric acidemia
Protein C deficiency


Findings in acute vs late abusive head trauma

- hemorrhage: retina, vitreous
- circular retinal fold
- papilledema
- optic nerve avulsion= ripped out of back of eye
- Intracranial hemorrhage

- optic atrophy, cortical damage (long-term)
- retinal detachment
- retinoschisis
- vitreous opacity
- subretinal scar
- central visual impairment (cortical blindness)
- amblyopia
- myopia


Treatment of shaken baby syndrome

Generally retinal hemorrhages resolve spontaneously
Close ophthalmologic follow-up
Some children need patching to prevent amblyopia
Some need surgical removal of vitreous blood
Watch for late Myopic shift!