Transcript CM-Ophtholmology lectures 1-7

There are 60 title slides
FULL LENGTH VERSION:
Answers to the pearls are highlighted in yellow,
but pertinent info has been included for completeness.
1.
2.
3.
Diagnosing amblyopia in children
Tests for visual acuity
Lateral light testing – differentials
1. Diagnosing amblyopia in
children… amblyopia is
discussed later too
Visual Acuity
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General physical examination should include :
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Visual acuity
Pupillary reaction – CN II, III
Extraocular movement – CN III, IV, VI
Direct ophthalmoscope – fundus, optic disc, retina
Dilated exam (in case of visual loss or retinal pathology)
Distance or Near
Distance visual acuity at age 3
 Early detection of amblyopia
 Early detection - key to correcting visual impairment
2. Tests for visual acuity
Distance Visual Acuity Testing
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OD - ocular dexter (right eye)
OS - ocular sinister (left eye)
OU - oculus uterque (both eyes)
VA - Visual Acuity (normal VA = 20/20)
 Calculation = Distance patient to eye chart / Distance at which the
letter can be read by a person with normal acuity
 If a patient’s VA is 20/40, it means this patient can read the 20/40
line from 20 feet away, WHEREAS a patient with normal VA (20/20)
can read that same 20/40 line from 40 feet away
 If a patient’s VA is 20/80, it means this patient reads the 20/80
line from 20 feet away, whereas a patient with normal VA (20/20)
can read that same 20/80 line from 80 feet away.
Distance Visual Acuity Testing
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Place patient at 20 ft from Snellen
chart
OD then OS
VA is line in which > ½ letters are read
Pinhole if < 20/40
Snellen eye chart
Distance Visual Acuity Testing
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If VA < 20/400
 Reduce the distance between the pt and the chart and record the
new distance (eg. 5/400)…have patient stand and walk closer to
the Snellen chart.
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If < 5/400,
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CF (include distance) – counts fingers @ 16” (inches)
HM (include distance) – hand motion @ 2’ (feet)
LP – light perception
NLP – no light perception
With above mentioned tests, try each one in order (if
patient cannot CF, attempt HM; if patient cannot see HM,
try LP)
Near Visual Acuity Testing

Indicated when
 Patient complains about near vision
 Distance testing difficult/impossible
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Distance specified on each card
(35cm)
Rosenbaum pocket chart
3. Lateral light testing – differentials
Pupillary Examination

Direct penlight into eye while patient
looking at distance
 Direct
○ Constriction of ipsilateral eye
 Consensual
○ Constriction of contralateral eye
Anterior chamber depth assessment
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Likely shallow if
 ≥ 2/3 of nasal iris in shadow
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2.
3.
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5.
Distinguish cataract types
Complications post cataract surgery
Medications for glaucoma
Open angle glaucoma epidemiology
Differentiating angle closure/narrow angle/open angle glaucoma
1. Distinguish cataract types
Cataract: Types of Opacifications
Types of cataracts:
1. Nuclear sclerotic (NS)
2. Cortical
3. Posterior subcapsular
(PSC)
Causes of cataracts
 Congenital
 Trauma
 Medications (i.e.
chronic steroid Tx)
 Systemic disease
 Age
***Nuclear Sclerotic (NS) Cataract***
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Most common
Yellowing of the central nucleus of the lens
Sclerosis - lens material becomes harder with
progression
Cortical Cataract
In the cortical layer of the lens
 Develop in the periphery of the lens and move inward
 Generally soft
 Look like spokes
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Cortical Cataract - Cortical Vacuoles
Vacuoles – look like air bubbles in glass
Cataract:
Posterior Sub-Capsular (PSC)
Generally begins in central vision
 Grow very quickly
 Common in patients with diabetes and prolonged steroid
use
 Cause significantly increased glare
 Very soft
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Cataract:
Posterior Sub-Capsular (PSC)
PSC – the white
blob in the posterior
aspect of the lens
Other causes of cataracts
 Congenital
 Trauma
 Medications
(i.e. chronic steroid Tx)
 Systemic disease
 Age
Congenital Cataract
Congenital Cataract

Any insult (e.g., infectious, traumatic, metabolic) to the
nuclear or lenticular fibers during lens formation may
result in an opacity (cataract) of the clear lenticular
media.
Congenital Cataracts
0.4% of births
 Not all congenital cataracts require surgical removal.
 Surgical removal indicated when involves the visual
pathway.
 Can cause permanent vision loss (amblyopia) if affects
vision and goes untreated.
 Opinions vary about implanting a lens implant due to eye
growth and development
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Traumatic Cataract
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Usually unilateral
Blunt or penetrating trauma
Other causes:
 Infrared energy (glass blower’s cataract)
 Electric shock
 Ionizing radiation
This one looks
like a palm tree
Steroids and Cataract
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Occurs in 50% of patients taking 10-15 mg daily for 2
years
Bilateral
May cause rapid visual changes
Posterior sub-capsular (PSC) cataract
Steroids also cause elevated
Intraocular Pressure (IOP)
Smoking and Cataract
Starting in 1982, epidemiologist William G. Christen of
the Harvard Medical School in Boston and his team
monitored 17,824 males who showed no sign of cataract
 In those males who smoked:
 200% increased risk of developing PSC cataract
 100% increased risk of developing nuclear sclerotic
cataract
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Diabetes and Cataract
60% more likely to develop cataract
 Tend to develop at a younger age
 Progress quickly
 Tend to heal more slowly after cataract removal
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Cataract: definition & symptoms
Characteristics:
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Not a growth or “skim” on
the eye
Prevents light rays from
passing clearly through
Usually progressively
worsens
Very common especially in
people over 55
Painless
Symptoms:
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Blurry, cloudy or smoky
vision
Increased glare
Yellowing of vision
Halos around lights at night
Difficulty reading or diving
Difficulty performing
activities of daily living
2. Complications post cataract
surgery
Cataract Surgery Outcomes
95% achieve 20/40 vision or better
 Infrequent complications
 Infection
 Bleeding (hemorrhage)
 Glaucoma
 Cystoid Macular Edema (CME)
 Retinal detachment (RD)
 Capsular bag opacification (Post Capsular Opacification)
 requires Nd:YAG laser capsulotomy in up to 50%
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3. Medications for glaucoma
MEDICAL TREATMENT OF GLAUCOMA…
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Beta blockers (Timpotic, Betoptic, Betagan, Betimol,
OptiPranolol)
Adrenergic agonists (Brimonidine, Propine)
Prostaglandin analogs (Travatan, Lumigan, Xalatan)
Carbonic anhydrase inhibitors (Azopt, Trusopt, Diamox{PO})
Cholinergic agonists—not used for primary therapy due to side
effects (Pilocarpine, carbachol)
Many come as combination agents (Combigan, Cosopt)
SIDE EFFECTS ARE MORE COMMON IN ELDERLY PATIENTS….
MUST BE AWARE OF THESE MEDICATION SIDE EFFECTS
Okay, he used lots of trade names in
the last slide,
In the next slides, the names are as
follows:
generic name (brand name)
So generic is highlighted yellow…brand
name is in parentheses
TOPICAL BETA BLOCKERS (BID) “-olol”
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Timolol (Timpotic, Betimol), Betaxolol (Betoptic), Levobunolol
(Betagan), Metipranolol (OptiPranolol)
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First line of glaucoma therapy before prostaglandins
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THIS IS THE OPPOSITE OF WHAT DR. ABLES SAID; BOTH CLASSES ARE EFFECTIVE DROPS.
Still highly useful for many patients (low cost, blue eyes)
 Side effects
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Dry eye
Impotence
Depression, confusion
Bradycardia
Bronchospasm - COPD
Congestive heart failure
Exacerbation of myasthenia gravis
TOPICAL ADERNERGIC AGENTS (TID)
Brimonidine (Alphagan P) may have neuroprotective properties
 Side effects:
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 Red eyes (toxic conjunctivitis) – Allergy to the preservative
 Headache
 Anxiety
 Tremor
 Increased BP (tachycardia)
 Tachyarrhythmia
TOPICAL PROSTAGLANDIN ANALOGS (QHS)
– “prost”
Travaprost (Travatan Z), Bitamoprost (Lumigan), Latanoprost
(Xalatan)
 Modern first line glaucoma therapy and convenient dosing
 Contraindicated for inflammatory etiology, history of herpetic eye
disease, or chronic iritis
 Side effects:
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Ocular irritation
Minimal systemic effects
Irreversible iris darkening (blue  brown eye)
Growth of eyelashes (Latisse)
CARBONIC ANHYDRASE INHIBITORS “-amide”
Brinzolamide (Azopt), Dorzolamide (Trusopt), Diamox{PO})
 ADJUNCT - Topical agents used in combination with other
medications
 Diamox PO for acute angle closure
 Side effects:
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 Malaise, anorexia, depression
 Serum electrolyte imbalance
 Renal calculi
 Blood dyscrasias
 Taste abnormalities, tingling of digits (PO form)…parasthesias
TOPICAL CHOLINERGIC AGENTS –”pine”
Pilocarpine – used for acute angle closure glaucoma
 Oldest class of glaucoma medications
 Generally not used for long-term therapy because of side
effects
 Side effects:
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 Brow ache
 Increased bronchial secretions
 Diarrhea
 Nausea, vomiting
 Apnea
4. Open angle glaucoma
epidemiology
RISK FACTORS FOR GLAUCOMA
African heritage
 Advanced age
 Family history
 Diabetes?
 Myopia
 Thin cornea
 IOP >21 mmHg
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Optic nerve cupping or
cupping asymmetry
 Cataract
 Pigment dispersion
 Narrow anatomical
angle
 Sleep apnea
 Prior ocular trauma
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5. Differentiating angle closure /
narrow angle / open angle glaucoma
5a. Angle closure
ANGLE CLOSURE GLAUCOMA (ACG)
Risk Factors:
 Increased incidence with age
 Female > male
 Hyperopia
 More common in some Asian populations
 Less common in some Caucasian groups
***ACG: SYMPTOMS***
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Severe pain
Decreased vision, halos
Headache, nausea, vomiting
Red eye, hazy cornea
Mid-dilated, irregular, non-reactive pupil
Worse in dim environments
IMMEDIATE TREATMENT AND REFRRAL INDICATED!
ACG: TREATMENT
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Medical treatment
 Topical beta blockers
○ “-olol” = timolol, betaxolol
 Topical cholinergic agents
○ “-pines” = pilocarpine
 Oral carbonic anhydrase inhibitors (Diamox PO)
 Oral osmotic agents
 Topical steroid
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Surgical treatment
 Laser iridotomy (PI)
5b. Narrow angle glaucoma
Narrow Angle Glaucoma
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Mechanism of ONH (optic nerve head) damage is from IOP
spikes during intermittent angle closure
Reduced aqueous outflow
Treated as POAG (primary open angle glaucoma)
May benefit from PI (peripheral iridotomy)
May be exasperated by certain systemic medications:
 Antihistamines – diphenhydramine (benadryl), loratidin (claritin)
 Decongestants - Pseudophedrine containing agents (Pseudofed)
 Polyuria drugs - detrol
5c. Open angle glaucoma
POAG - Primary Open Angle Glaucoma
POAG: PATHOPHYSIOLOGY
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Outflow obstruction
Increased intraocular
pressure (IOP)
 Damage to nerves
 Decreased peripheral
vision
 Tunnel vision
Normal = 0.30
Glaucomatous = 0.75
POAG: MEDICAL Tx
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Medical therapy goals
 Halt visual field loss
 Prevent further optic nerve
damage
 Lower IOP
 Assess visual fields at least once
a year
POAG: SURGICAL THERAPY
Laser therapy (SLT, ALT)
 Filtering surgery (bleb)
 Placement of drainage device (valves)
 Cyclodestructive surgery of ciliary body
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1.
2.
3.
4.
Organisms involved with eyelid infections
Eyelid tumor etiologies
Facial Herpes zoster complications
Distinguish retinal vein occlusion / cataract / DM retinopathy / vitreous
detachment
1. Organisms involved with eyelid
infections
BLEPHARITIS…staph aureus
‘Granulation of the eyelids’
 Staphylococcus aureus overgrowth thought to be
cause
 No cure, symptoms wax and wane over time
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2. Eyelid tumor etiologies
EYELID CANCER
Biopsy indicated in suspicious lesions
 Surgical treatment warranted
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 Basal Cell Carcinoma (BCC)
○ Most common malignant eyelid tumor
 Squamous cell carcinoma
 Sebaceous carcinoma
 Melanoma
3. Facial Herpes zoster complications
HERPES ZOSTER OPHTHALMICUS
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Reactivation of HZV in the Fifth Cranial Nerve; usually
spares lids and eyes
Treat with oral antiviral
Hutchinson’s Sign (lesion on tip of nose) indicates eye
involvement (nasociliary branch of trigeminal nerve)
 keratitic dendrites, conjunctivitis, uveitis possible

referral if eye involvement suspected
 Treatment may include artificial tears, erythromycin ointment,
topical steroid, cycloplegia, glaucoma meds
4. Distinguish retinal vein occlusion /
cataract / DM retinopathy / vitreous
detachment
4a. Retinal vein occlusion
CENTRAL RETINAL VEIN OCCLUSION (CRVO)
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Painless unilateral loss of vision
 Ischemic CRVO: VA worse than 20/400 +APD
 Nonischemic CRVO: VA better than 20/400 –APD
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Diffuse retinal hemorrhages in 4 quadrants;
dilated, tortuous retinal veins
CRVO TREATMENT
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Change diuretics to other antihypertensive
medications, if possible
Treat IOP if elevated
Treat underlying medical disorders
Monitor carefully for neovascular glaucoma (90
day glaucoma)
8-10% risk of developing CRVO or BRVO in
fellow eye
BRANCH RETINAL VEIN OCCLUSION (BRVO)
Similar to CRVO, only involving a sector of
the retina
 Partial loss of visual field

OTHER RETINAL
PATHOLOGIES that he
harped on in class
AION (arteritic ischemic optic
neuropathy)
GIANT CELL ARTERITIS (GCA)
AKA: Temporal arteritis, Cranial arteritis,
etc.
 Vasculitis affecting medium sized arteries
 Can cause
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ischemic optic neuropathy
cranial nerve palsies (6th nerve)
retinal vascular occlusions
blindness
stroke
death (aortic aneurysm)
GCA: SYMPTOMS…clinical Dx
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CF or worse vision
+APD
headaches
malaise
night sweats
weight loss
jaw claudication
scalp tenderness
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50% have symptoms
of polymyalgia
rheumatica
transient visual
disturbances in weeks
or months preceding
age > 50 years
GCA: DIAGNOSIS
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Classic clinical symptoms
15% incidence in polymyalgia rheumatica patients
Elevated sed rate (ESR)
 Not specific or sensitive
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Elevated C-Reactive Protein (CRP)
 More specific for GCA than elevated ESR alone
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Temporal artery biopsy (TABx)
 giant cell and granulomatous infiltration of the intima of
medium sized-arteries
 5 % false negatives due to skip lesions
 Biopsy should be performed in ANY suspected case of
GCA
GCA: TREATMENT
Immediate IV steroids once suspected
 Risk of attack in other eye if untreated
 TABx should be performed within 10 –
14 days of treatment
 May require 6-12+ months of oral
steroids if diagnosis positive
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CENTRAL RETINAL ARTERY
OCCLUSION (CRAO)
Sudden painless total loss of central and
peripheral vision (CF to LP vision)
 Pale fundus with cherry red spot at macula
 This is a stroke of the eye
 CRAO is a true eye EMERGENCY
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 Opportunity to treat is 90 minutes after occurrence
(compression gonioscopy, decrease IOP, carbogen)
4b. Cataract
CATARACT
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Lens opacification results from aging damage to the
lens proteins
4c. DM retinopathy
STAGES OF DIABETIC RETINOPATHY
Mild NPDR – some bleeding, some vascular changes
Moderate NPDR – some focal edema, more hemorrhage, veins
Severe NPDR – macula significantly involved, macular edema, refer to retinal specialist
PDR – angiogeneis/neovascularization  macular edema
4d. Vitreous detachment
VITREOUS ABNORMALITIES
Posterior Vitreous Detachment (PVD)
 Vitreous gel breaks down over time
 “FLOATERS” = debris in vitreous (worse on paper, worse
looking at blue sky)
 Etiology - partial PVD

Vitreous separates from retinal tissue (PVD)
 “FLASHES” – PVD  can get retinal traction  flashing
lights in periphery
 Rods –
○ Cells are programmed to see OR not see light; no other
function 
○ Explains why patients c/o symptom - FLASHES OF LIGHTS
1.
2.
3.
4.
Treatment for bacterial conjunctivitis
Treatment for “stye”
Distinguish episcleritis/scleritis/glaucoma/subconjunctival
hemorrhage
Cellulitis involving the eye and surrounding structures
1. Treatment for bacterial
conjunctivitis
Types of Conjunctivitis
Bacterial
 Viral
 Allergic
 Neonatal (gonococcal)
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Bacterial Conjunctivitis
Mild to moderate sticky purulent discharge
 Contagious
 Crusty eyelids and eyelashes in the
morning
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Bacterial Conjunctivitis: Common Causes
Staphylococcus (skin)
 Streptococcus (respiratory)
 Haemophilus (respiratory)
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Bacterial Conjunctivitis: Treatment
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Topical antibiotic: 4 times/day x 7 days
 Polytrim (Trimethoprim/polymyxin B)
 Fluoroquinolones ($$)
 Bacitracin (available in ointment)
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Warm compresses
Gonococcal Conjunctivitis
Severe purulent discharge
 Hyperacute onset
 Palpable preauricular node
 Eyelid swelling
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Neonatal Conjunctivitis
Bacteria (gonorrhea, appears in 2-4
days)
 Bacteria (Staphylococcus,
Streptococcus, appears in 3-5 days)
 Chlamydia (appears in 5-12 days)
 Viruses (e.g., herpes from mother)
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Gonococcal Conjunctivitis: Treatment
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Risk for rapid corneal perforation
IM antibiotics
Topical bacitracin or ciprofloxacin
Eye irrigation QID until discharge eliminated
Possible coinfection with chlamydia
Identify and treat sexual partners
2. Treatment for “stye”
Hordeolum (Stye)
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Acute, palpable, well-defined, subcutaneous nodule in the
eyelid
Tender to touch
Treatment: use warm compresses with lid massage QID for
10 minutes
Chalazion
• Long-standing, palpable, well-defined, subcutaneous nodule in
the eyelid
• No pain/discomfort
• Treatment: warm compresses with lid massage QID for 10 min,
if no improvement after 3-4 wks, consider excision
• Exc of chalazion
3. Distinguish
episcleritis/scleritis/glaucoma/
subconjunctival hemorrhage
Scleritis vs. Episcleritis
Scleritis
Episcleritis
Diffuse or sectorial
Sectorial
Severe and boring eye pain
Mild-moderate tenderness
BV do NOT blanch with phenylephrine
BV blanch with phenylephrine
Gradual onset
Acute onset
Sclera has bluish hue
Young age, mild symptoms
50% associated with systemic disease Idiopathic (most common)
(eg. RA, Wegener granulomatosis, AS,
Reiter’s, lupus, polyarteritis nodosa)
Tx: oral NSAIDs, systemic steroids,
**topical steroids are NOT effective**
Tx: AT’s QID or mild topical steroid
(FML or Lotemax) QID, oral NSAIDs
Scleritis and Episcleritis
Scleritis
Episcleritis
3a. Episcleritis
3b. Scleritis
3c. Glaucoma
Angle Closure Glaucoma
Bottom right
• Angle of iris vs. cornea
• Narrow angle glaucoma
• Sx
• PAIN
• Hazy cornea
• Elevated IOP 45-60mmHg
• Dx = gonioscopy
• Tx = YAG PI (peripheral iridotomy)
3d. Subconjunctival hemorrhage
Subconjunctival Hemorrhage
4. Cellulitis involving the eye and
surrounding structures
Orbital vs. Preseptal Cellulitis
Orbital Cellulitis
Preseptal Cellulitis
Pain with eye movement
Eyelid edema
Fever
NO fever
Diplopia
NO diplopia
Proptosis
NO proptosis
EOM restriction
NO EOM restriction
Redness and eyelid edema
Redness
Decreased vision
Vision not affected
Preseptal Cellulitis
Eyelid erythema and edema
 Tenderness of the eyelid and periorbital area
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• NO proptosis, NO EOM restriction, NO pain with eye
movement
Ocular Emergency!!
Symptoms of Orbital Cellulitis
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Redness and swelling
EOM restriction
Pain with eye movement
Double vision (diplopia)
Fever
+/- proptosis
+/- optic nerve: decreased vision, afferent
pupillary defect, disc edema
Precipitating Factors
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Penetrating lid trauma
Direct extension from
sinus infection
Blow-out fracture
Severe orbital infections
Bite wounds
Meningitis
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Sinusitis and sinus
infection
Septicemia
Ketoacidosis
Strabismus surgery
Retinal surgery
Dental abscess
Treatment of Orbital Cellulitis
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Requires in-patient care with parenteral
antibiotics
Blood culture
Orbital CT scan
ENT consult if pre-existing sinus disease
Surgical debridement if caused by fungus, no
improvement, or subperiosteal abscess
Topical and oral antibiotic therapy will not help!
Orbital Cellulitis CT scan
Orbital Cellulitis
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2.
3.
4.
Treatment for globe trauma
Foreign body presentations on/in the eye
Treatment for corneal abrasions
Seidel’s test
1. Treatment for globe trauma
OCULAR TRAUMA
Corneal abrasion
 Chemical Burns
 Blunt Trauma
 Foreign Body
 Globe Trauma
 Eyelid Trauma

**Treatment for ocular
trauma should be
instituted IMMEDIATELY!
**Treat the patient
BEFORE testing vision
RUPTURED GLOBE
Defined: Any full-thickness injury to the
sclera, cornea or both; caused by blunt
trauma
 Signs:
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Severe subconjunctival hemorrhage
Hyphema
Peaked pupil
EOM restriction
Decreased vision
Fluid leak, history consistent with rupture
RUPTURED GLOBE
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Work-up/Treatment
Avoid placing pressure on the globe
Protect the eye with a shield
Immediate referral to ophthalmology
Admit patient to the hospital with no food or drink
Immediate surgery indicated
 Prognosis depends upon extent of injuries
 CT Scan to r/u intraocular FB and localize the rupture site
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2. Foreign body presentations
on/in the eye
FOREIGN BODY
History of trauma, tearing, and pain/discomfort
 Need slit lamp exam to determine presence of foreign body
 If foreign body is present, obtain careful history to determine
mechanism of injury
 Intraocular foreign body
*emergency referral*

 especially if metal against metal
 high velocity impact
 positive Seidel sign
 Order X-ray, B-scan, or CT scan to help rule out
 Avoid MRI
FOREIGN BODY REMOVAL
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Remove with spud, Q-tip, needle, etc.
Use magnified vision, not naked eye
Get ALL of it out, or everything but rust ring
Use algerbrush for rust ring
Spud
Needle > 24 hrs
Burr
Algerbrush
FOREIGN BODY
Once FB is removed, treat like a corneal abrasion
 Treat with topical antibiotics
 Option to patch or use bandage contact lens
 Follow up daily if patched or if abrasion is large
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SEIDEL’S TEST
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Very important to perform this test whenever there is a
possibility of an intraocular foreign body
Essentially, if there is a FB or corneal abrasion, the fluorescein
stain will leak through the cornea as a BLACK color.
Checks for anterior chamber leakage into the cornea
http://www.youtube.com/watch?v=GlFcAv0DR4c
http://www.youtube.com/watch?v=w9GIxsjEfBk
3. Treatment for corneal
abrasions
CORNEAL ABRASION
•
•
Defined: An epithelial defect of the cornea
Symptoms:
•
•
•
•
•
Pain
Photophobia
FB sensation
Tearing
History is important!
• Superficial vs. penetrating
• Find out what happened
• Consider topical anesthetic, IN-OFFICE ONLY!
CORNEAL ABRASION

Work-up:
 Evaluate under slit lamp
 Use fluorescein dye
 Measure the size
 Evaluate for A/C reaction
 Evert eyelid to r/o FB
CORNEAL ABRASION TREATMENT

Antibiotics
 Ointment vs. Drop
○ Ointment better for kids but blurs vision
○ Ointment: Use Bacitracin or Erythromycin Q2-4 hours
○ Drops: Use Polytrim, Tobramycin, or Fluoroquinolone QID

Cycloplegics
 Helps w/ discomfort from traumatic iritis (can develop 24-72 hrs after
trauma)

Pressure patching
 Consider for comfort
 DO NOT PATCH: vegetation, CL patient, false fingernails

NSAID drops for pain
 Ketoralac QID for 3 days
CORNEAL ABRASION TREATMENT
Antibiotic
Cycloplegic
NSAID
4. Seidel’s test
SEIDEL’S TEST
Very important to perform this test whenever there is a
possibility of an intraocular foreign body
 Essentially, if there is a FB or corneal abrasion, the
fluorescein stain will leak through the cornea as a BLACK
color.
 Checks for anterior chamber leakage into the cornea



http://www.youtube.com/watch?v=GlFcAv0DR4c
http://www.youtube.com/watch?v=w9GIxsjEfBk
1.
2.
3.
4.
Distinguish amblyopia / astigmatism / hyperopia / myopia /
strabismus
Forms of amblyopia
Red reflex abnormalities
Define exotropia
1. Distinguish
amblyopia/astigmatism/hypero
pia/myopia/strabismus
1a. Amblyopia
Amblyopia – “Lazy” eye
Definition: loss of vision in one or both
eyes caused by conditions that impair the
visual input to the brain during the period
of development of vision
 Eye(s) often anatomically normal – at least
to superficial inspection

1b. Astigmatism
Astigmatism
Defect in the eye or in a lens caused by a
deviation from spherical curvature, which
results in distorted images,
 Light rays are prevented from meeting at a
common focus (retina, fovea centralis)
 Thus, vision is blurry

1c. Hyperopia
Hyperopia
Farsightedness
 Distance vision is good
 Near vision is not as good
 Eye is too short, so light rays converge on
a spot behind the retina

1d. Myopia
Myopia
Nearsightedness
 Distance vision is poor
 Near vision is good
 The eyeball is too long, so light rays
converge at a point in front of the retina

1e. Strabismus
Strabismus
Misaligned eyes
 Esotropia: turning IN
 Exotropia: turning OUT
 Hypertropia: turning UP
 Hypotropia: turning DOWN

Strabismus
Constant or intermittent
 Constant: tropia
 Tendency: phoria

Strabismus
Comitant vs Incomitant
 Comitant: ~same deviation in all positions
of gaze
 Incomitant (often a neurological etiology –
eg. CN VI palsy): deviation will differ in
different positions of gaze

ESOtropia
Turning IN
 First few months to years of
life
 Diagnose with the corneal
light reflex test or cover test
 REFER

EXOtropia





Turning OUT
Usually diagnosed between
2-4 years of age
Usually intermittent (at least
at first)
Corneal light reflex or cover
test
REFER
HYPERtropia / HYPOtropia
HYPER: eye turns UP
 HYPO: eye turns DOWN
 Corneal light reflex test, cover test
 REFER

Pseudostrabismus
A false appearance of misalignment
 Cover test
 Consider referral

Pseudostrabismus/esotropia


Wide nasal bridge
 false appearance
Cornea light reflex is
the same
2. Forms of amblyopia
Amblyopia – types – the 3 Ds
Deprivational
 Deviated
 Defocused

Amblyopia -- Deprivational

Anything that obstructs the line of sight during
the first few years of life (?up to age 9)
 Droopy lid (ptosis), cataract, tumor
The most severe form of amblyopia
 Tx:

 Treat the underlying disorder
 Then treat the amblyopia
Amblyopia -- Deprivational
Amblyopia -- Deviated
Misalignment of an eye (strabismus) leads
to suppression and then poor vision from
amblyopia in the first few years of life
 Both the amblyopia and the strabismus
need to be treated

Amblyopia -- Deviated
Amblyopia -- Defocused
Usually when one eye is out of focus when
compared to the other eye eg. One eye
severely hyperopic (farsighted), the other not
 Can occur in both eyes if the refractive error is
severe
 Usually the least severe form of amblyopia

 Difficult to Dx from inspection
 VA might give it away
Amblyopia -- Defocused
Amblyopia -- Treatment
Treat the underlying cause if possible
 Glasses (contact lenses)
 Patching the good eye

 Trains poor eye to improve VA

Drop treatment – atropine penalization
 7-14 days – blue eyes; blurring wears off 2-3 days
 <7 days – brown/dark eyes; blurring wears off 1-2 days
Amblyopia -- Treatment
3. Red reflex abnormalities
***Retinoblastoma***
Most common intraocular malignancy in
childhood
 1/15, 000
 May be inherited (autosomal dominant)
 Tumor of the photoreceptors

Retinoblastoma -- Presentation
Abnormal red reflex – WHITE
 Misaligned eye
 Iris heterochromia
 Red, swollen eye

Retinoblastoma -- Management

REFER
 24-48 hrs
Confirmation, referral on to a specialized
center
 Chemotherapy, radiotherapy, laser,
enucleation

4. Define exotropia
EXOtropia…repeat





Turning OUT
Usually diagnosed between
2-4 years of age
Usually intermittent (at least
at first)
Corneal light reflex or cover
test
REFER
1.
2.
3.
4.
DM eye changes
Diagnostic testing after noting optic nerve edema
Malignancy and the eye
Thyroid disease and the eye
1. DM eye changes
BDR vs. PPDR vs.
PDR
FOCUS on the first slide in each
subsection … the others
include images and
explanation
Vasculopathy
Diabetic Retinopathy
#1 cause of blindness of patients 20-64
 Pathologic mechanisms:

 capillary closure = ischemia
 increased permeability = edema
1a. BDR/NDPR – Background
Diabetic Retinopathy / Non
Proliferative Diabetic Retinpathy
BDR / NPDR (non-proliferative)

Microaneurysm
 Earliest clinically detectable lesion
 INL - Inner Nuclear Layer
Hard Exudate: ONL - Outer plexiform layer
 Retinal Edema

 Initially OPL and INL, then IPL and NFL, then all

Hemorrhage
 Intraretinal: venous source- dot blot hem
 NFL - Nerve Fiber Layer: superficial arteriole- flame hem.
1a. Background Diabetic Retinopathy (BDR)
microvascular changes confined to the retina and do not extend beyond the internal
limiting membrane
Microaneurysm
Tiny, round, red dots, first appear temporal to fovea
Earliest clinically detectable lesion
Inner Nuclear Layer
Hard Exudate
Waxy, yellow lesions with relatively distinct margins
Circinate exudate often with microaneurysm
Outer plexiform layer
FA: hypofluorescence due to blockage of choroid
Retinal Edema
Initially found between OPL and INL, then IPL and NFL
FA late hyperfluorescence due to capillary leakage
Hemorrhage
Intraretinal = dot-blot: venous origin, middle layers
NFL = flame hem: arteriole origin, NFL
FA: hypofluorescence due to blockage of choroid
1b. PPDR – Pre Proliferative
Diabetic Retinopathy
PPDR: clinical features

Cotton wool spots:
 Focal infarcts of NFL due to arteriole occlusion

IRMA: intraretinal microvascular abnormalities
 AV shunts bypassing capillary bed (often occluded)

Venous changes
 Beading, dilatation, looping

Arterial changes due to atherosclerosis
 Narrowing, silver-wiring, obliteration like BRAO (branch retinal artery occlusion)

Dark Blot Hemorrhage
 Hemorrhagic retinal infarcts within middle layers
Cotton Wool Spot
• Small, white, fluffy superficial lesions that obscure underlying vessels
• Focal infarcts of NFL due to occlusion of arterioles
• Interruption of axoplasmic transport with subsequent buildup of transported
material gives white color
• FA: hypofluroescence due to blockage of choroid
IRMA
• Fine red lines that run from arterioles to venules
• AV shunts bypassing capillary bed often next to areas of capillary
closure
• Resemble neovasc’n but do not cross major blood vessels and no
leakage on FA
Venous changes
Tortuous - resistance of flow
Dark Blot Hemorrhages
PPDR- management
PPDR = pre-proliferative
diabetic retinopathy
Principal goal of BDR treatment is to prevent
progression to PDR
 PPDR should be watched closely because of the
risk of PDR
 Photocoagulation is usually not appropriate
unless regular follow-up is not possible, or
vision in the fellow eye has been already lost
due to proliferative disease
 ETDRS 4:2:1 rule defines Severe NPDR

1c. Diabetic Maculopathy
Diabetic maculopathy
Involvement of the fovea by: 1) edema, 2)
hard exudate, 3) or ischemia
 Most common cause of visual impairment
in diabetic patients, esp. DM II
 Exudative, ischemic and mixed forms

Diabetic maculopathy
Exudative DM maculopathy
• Retinal thickening assoc with rings of perifoveal hard exudate and/or
cystoid changes
• FA: late hyperfluorescence due to leakage, good macular perfusion
Ischemic DM maculopathy
• Reduced VA assoc with relatively normal appearing fovea
• FA: capillary non-perfusion at the fovea
1d. PDR – Proliferative Diabetic
Retinopathy
PDR = neovascularization






New vessels start as endothelial proliferations; most
frequently arising from veins
New vessels pass through defects in ILM to lie in potential
space between retina and post. vitreous
Posterior vitreous is scaffold for growth
NVD = within one disc diameter of ONH
NVE = neovascularization elsewhere
FA: fluroescence in early phases, hyperfluorescence and
leakage during late phases
Proliferative DM retinopathy
fibrovascular proliferation extends beyond the ILM and outside the retina
PRP
PRP - Pan-Retinal Photocoagulation
Laser therapy aimed at inducing involution of new vessels
1e. Advanced Diabetic Eye
Disease
Advanced Diabetic Eye Disease
Two main sequelae:
1) Hemorrhage
2) Tractional Retinal
Detachment

Contraction of fibrovascular
tissue over large areas of
vitreoretinal adhesion
PPV is the mainstay of treatment
for advanced disease
PPV = pars plana vitrectomy
2. Diagnostic testing after noting
optic nerve edema
Scan Before You Tap!!!
CT before You LP

Optic Nerve Edema is
Intracranial Mass
until proven
otherwise!!!

Don’t herniate the
brainstem
3. Malignancy and the eye
The eye gets cancer, too
but it’s usually from somewhere else
90% go to the choroid
 Blurred vision is most
common visual
symptom

 But often no visual
symptoms

M. Common primary
women: breast
men: lung/bronchus
Metastatic cancer  goes to the eye
Ocular metastasis

Patient survival
generally poor
 Median 8-12 months
overall
 Breast cancer 15-17
months

Poor prognosis
4. Thyroid disease and the eye
Thyroid Eye Disease

Autoimmune disorder
 Ig that stimulates TSH-
receptors on orbital fibroblasts

Usually hyperthyroid
 but may be hypo-, or euthyroid

Characteristic signs:




Eyelid retraction
Proptosis
Restricted EOM
Optic neuropathy

Eyelid retraction pic,
m.common
Thyroid Eye Disease

M. common cause of
proptosis
 Unilateral, or
 Bilateral

Inferior and medial rectus
muscles m. common
 Spares the tendons
Thyroid Eye Disease Treatment



No Smoking
Normalize thyroid levels
Eye specific Tx:



Lubricate w/ ATs
Decrease inflammation w/ Pred Forte
* Increase Orbital Space w/ surgery - orbital decompression

Allowing contents to prolapse into ethmoidal and maxillary sinus to relieve congestion in the
orbital space