Optho Flashcards
1
Q
Layers of eye
A
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
2
Q
Chambers of eye
A
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)
3
Q
Development of eye
A
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
4
Q
Organization of Retina
A
OUTERMOST 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 INNERMOST
Basic layers:
- Retinal pigment epithelium
- Photoreceptors= phototransduction (light to neural activity)
- Interneurons= process neural signals
- Ganglion cells
Specializations of retinal layer:
- Optic disk/papilla (optic nerve, blind spot)
- When looking at something, blind spot in one eye compensated by other side/brain - 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 - Ora serrata:
- Anteriormost border of neural retina
- 10 layers collapse to 2= pigmented epithelium (no rods, cones, ganglion)
5
Q
Organization of anterior eye (choroidal layer, corneo-scleral layers)
A
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
6
Q
Anterior Chamber angle of eye
A
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
7
Q
Organization of Iris
A
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)
8
Q
Organization of cornea
A
Five layers:
- Stratified squamous non-keratinized corneal epithelium
- Bowman’s (basement) membrane
- Regular connective tissue= substantia propria (stromal layer)
- Descemet’s (basement) membrane
- Simple squamous corneal endothelium
9
Q
Organization of lens
A
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
10
Q
Organization of eyelid
A
Protects exposed surface of eye
- Outer surface= thin skin
- Inner surface= conjunctiva (stratified columnar epithelium with goblet cells)
Contains:
- Tarsal plate (fibroelastic connective tissue)
- Orbicularis muscle
- Large sebaceous Meibomium glands
- Small sebaceous Zeis glands
- Moll sweat glands
11
Q
Lacrimal glands
A
Secrete tears
- Tubulo-alveolar serous glands
- Large lumens, few ducts
- Looks similar to pancreas (no Islets of Langerhans)
12
Q
Diabetic retinopathy: mechanisms of hyperglycemic damage
A
Diabetic retinopathy= microvascular disease due to chronic hyperglycemia
Mechanisms:
• 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
13
Q
Earliest findings of capillary damage
A
- Thickened basement membranes
- Pericyte dropout
- Pericytes are contractile cells which regulate flow through capillaries - Microaneurysms
- Degenerate and leak
- See hard exudates, macular edema
14
Q
Non-proliferative Diabetic Retinopathy (NPDR)
A
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
15
Q
Proliferative Diabetic Retinopathy
A
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
16
Q
Symptoms of macular edema
A
- 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
17
Q
Predictors for severity of diabetic retinopathy
A
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.
18
Q
Prevention of diabetic retinopathy
A
• 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
19
Q
Focal Laser treatment
A
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%
20
Q
Other treatments for diabetic non-proliferative retinopathy
A
- Intravitreal corticosteroids
• Injections (triamcinolone)
• Implants (fluocinolone, dexamethasone + PLGA intravitreal delivery for 35 days)
- Complications: increased IOP, endopthalmitis (infection), cataracts - 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 - Parsplanavitrectomy (remove vitreous humor)
21
Q
Treatment of Proliferative diabetic retinopathy
A
- Panretinal laser photocoagulation
- Apply laser to entire midperipheral fundus
- Complications
• Slight decrease in vision
• Slight decrease in night vision
• Slight decrease in peripheral vision - Vitrectomy surgery
- Used in patients with non-clearing vitreous hemorrhage
- Tractional retinal detachment
- Complications: major procedure, eyes/patients have poor risks, costly
22
Q
Tractional Retinal Detachment
A
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)
23
Q
Causes of Red Eye
A
- Conjunctivitis
- Discharge - Keratitis (inflammation of cornea)
- may have discharge
- Painful
- Decreased vision
- pupil size may change - Iritis
- Painful
- may have Decreased vision
- Unequal pupil - Acute angle closure glaucoma
- Painful
- Decreased vision
- Dilated pupil
Uncommon:
- Pterygium
- Episcleritis
- Scleritis
- Dacryocystitis
24
Q
Conjunctivitis
A
Chief complaint: foreign body sensation
Types:
- 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 - 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) - 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
Treatment:
- 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
25
Red eye in infants
- Ophthalmia neonatorum (neonatal conjunctivitis)
- Dacryocystitis
- Congenital glaucoma
Causes:
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)
Prophylaxis:
- Erythromycin ophthalmic ointment
- Azithromycin gel drops
26
Chronic conjunctivitis
```
Chlamydia
Blepharitis
Toxic (medications)
Molluscum contagiosum of the eyelids
Allergic (seasonal or vernal/atopic)
Factitious
```
27
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
Treatment:
- Systemic tetracyclines, azithromycin, erythromycin for 3-6 weeks
28
Blepharitis
Inflammation of the eyelid margin
- Crusting of the eyelashes, typically worse in the morning
- Associated with dry eyes
- Clogged Meibomium glands (zits)
Treatment:
- Warm compresses
- Eyelid scrubs, antibiotic ointment
- Occasionally systemic tetracyclines, azithromycin
29
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
30
Corneal problems
```
Trauma
- Foreign bodies
- Chemical burns
Contact lens complications
Bacterial ulcers
Herpes simplex virus infections
Other infections
- (e.g. fungus, acanthamoeba, herpes zoster)
```
31
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)
32
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
33
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
34
Iritis
Signs/symptoms: circumcorneal injection, photophobia
Secondary to blunt trauma, keratitis
Associated with systemic diseases (e.g. sarcoidosis, connective tissue disorders)
Idiopathic
35
Referral not necessary for following:
Conjunctivitis improving over 2-4 days
Tx: cool compresses and tears
Chalazion
Tx: warm compresses
```
Subconjunctival hemorrhage (nontraumatic)
Tx: none
```
36
Steroid complications in eye
Glaucoma (in susceptible patients)
Cataract (dose related)
Enhances most active infections, especially:
- Herpes simplex infections
- Fungal infections
- Acanthamoeba infections
37
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
38
Vascular supply to eye
Choroidal artery= back of retina
| Retinal artery, vein
39
Retinal vascular disease
- Artery Occlusions
- Vein Occlusions
- Hypertension/ Arterial Sclerosis
- Amaurosis Fugax
- Ocular Ischemic Syndrome
- Diabetes Mellitus
- Sickle Cell Disease
40
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)
41
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
42
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)
43
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
```
```
Causes:
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
44
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
Causes:
- Atherosclerosis (Majority)
- Arterial spasm (e.g. migraine)
- Dissecting aneurysm
- GIANT CELL ARTERITIS= 1% of cases (rare, but can become bilateral quickly)
Management
- 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
45
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)
Management:
1. Macular edema
- Laser
- Intravitreal triamcinolone or antiVEGF agent
2. Neovascularization
- PRP to ischemic area
46
Central Retinal Vein Occlusion
```
= Dilated and tortuous retinal veins all 4
quadrants
- Optic disc swelling
- Intra-retinal hemorrhages
- Macular edema
- Cotton-wool spots
```
Pathogenesis:
- 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)
Management:
- Family medical doctor to manage
- Hypertension
- Diabetes
- Elevated cholesterol
Treatment:
- Neovascularization: Laser (panretinal photocoagulation- permanent, shirinks vessels)--> avoid glaucoma by catching before vasculature moves into angle
- Macular edema: Intravitreal triamcinolone; Anti VEGF agents (temporary)
47
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
Pearls:
- 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!
48
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
49
Ocular Ischemic Syndrome
>90% ipsilateral carotid artery obstruction
- Relatively rare clinical entity
Symptoms
- None
- Visual loss over weeks to months
- Periorbital aching pain
Signs:
- Rubeosis iridis (iris neovascularization)
- Dilated but not tortuous retinal veins
- Mid-peripheral retinal hemorrhages
Prognosis: Poor
- 40% five year mortality
- Stroke and cardiac events
Treatment:
- Laser for rubeosis
- Carotid endarterectomy/stent
Resembles central artery occlusion, but arteries straight not tortuous
* High risk for stroke, other ischemic events
50
Sickle cell retinopathy
Clinical features- Spectrum like diabetes
Background:
- Salmon patch- acute intraretinal hemorrhage
- Black Sunburst- subretinal pigment clump
Proliferative:
- Sea fan- peripheral retinal neovascularization
- Vitreous hemorrhage
- Traction retinal detachment
Causes (in descending order):
- Hgb SC
- Hgb Sthal
- Hgb SS
- Hgb AS (trait)
Treatment:
- Laser therapy for proliferative sickle disease (promotes regression)
51
Retinopathy of prematurity
Demographics:
- 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)
Diagnosis
- Screening exams in NICU
- Babies born <20%
52
Optic neuropathy: signs
+/- decreased acuity
- RAPD (relative afferent pupillary defect) if asymmetric
- Dyschromatopsia= color vision problems
- Optic nerve may be: swollen, normal, pale
53
Optic neuritis
Presentation:
- Younger patients (20s-30s)
- Female > Male
- Caucasian, Northern European
- Pain with eye movement (92%)
- Vision loss progressing over 1-2 weeks
Signs:
- 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)
Diagnosis:
- 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
54
Anterior ischemic optic neuropathy:
| Non-arteritic
Optic nerve affected close enough to globe--> disc swelling (hence anterior)
- Common features: acute vision loss, disc edema
Features:
- Younger age (60s, 70s)
- Vasculopathic risk factors
- No warning symptoms
- No treatment
History:
- Sudden vision loss
- Often upon awakening
- Stable from onset
- May have mild pain
- No prodrome
Risk factors:
- HTN
- DM
- Elevated cholesterol
- Smoking
- Sleep apnea
- ED drugs
Signs:
- 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)
Prognosis:
- 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
55
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
Features:
- 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!
History/symptoms:
- 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
Signs:
- Relative afferent pupillary defect
- Dyschromatopsia (color loss)
- Visual field defects
- Normal appearing or Swollen nerve; “Chalky White”
Management:
- 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
56
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)
Pathophys:
- 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)
Imaging:
- Enlarged extra-ocular muscles SPARING TENDON where it inserts into eye
- Crowding at orbital apex
Treatment:
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!!
57
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
Signs/symptoms:
- Protosis (muscle inflammation)
- Pain- scleral involvement
- Double vision (diplopia)- muscles
- Loss of vision- nerve
- Red eye
Diagosis/treatment:
- Radiology may show enlarged muscles INCLUDING TENDONS (vs TRO)
- Biopsy if atypical
- VERY responsive to steroids
58
Ocular Myasthenia Gravis
Autoimmune reaction affecting NM junction
- Reduced number of Ach receptors due to auto-antibodies against receptors
Symptoms:
- Generalized weakness
- Ocular only: “Ocular Myasthenia Gravis”
- Fatiguable muscular weakness
- Eyelids/extraocular muscles involved in > 90% (double vision, ptosis= variable, fatiguable)
Diagnosis:
- 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
Treatment:
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
59
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
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Strabismus
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
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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
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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
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Comitant Strabismus: Accomodative Esotropia
- Develops age 1 -4
- Intermittent at first, increases over time
- Amblyopia common
Mechanism:
- 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
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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
65
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
66
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
67
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”.
Mechanism:
- Congenital
- Trauma
- Aneurysm
Treatment very difficult with only two working muscles, but some patients do well with surgery
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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
Treatment:
- 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
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Incomitant strabismus: CN6 palsy
Involves the lateral rectus muscle
Mechanism:
- 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
Treatment:
- Prism glasses for small degree of diplopia
- Surgical correction
- Many resolve on their own and do not require treatment
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Mechanical limitation of eye movement
Blowout fracture
| Orbital mass
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Ambylopia
Visual issue often occurring with strabismus
Causes:
- Refractive (49%)
- Strabismus( 49%)
- Ocular Pathology (2%)
1. Cataract
2. Glaucoma
3. Corneal anomaly
Treatment:
- 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
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Patching
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
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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).
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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
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Central vision
Measure of macular function
- Measures two disc diameters from optic nerve to temple
- Measured with Snellen chart
76
Refraction
Elements of refractive errors:
77
Diopter
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)
78
Emmetropia
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
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Myopia
Near-sighted
Parallel light rays focused in FRONT of fovea
- Retina presented with diverging rays
Causes:
- Increased corneal curvature
- Longer axial length
- Increased refractive index of lens due to nuclear sclerosis
Symptoms:
- Blurred distance vision
- Squinting (pinhole effect): narrowing aperture to decrease refraction
- Holding reading close
Correction:
- Divergent (concave) lens
Ex: +64.00 Diopter eye corrected by -4.00 lens
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Hyperopia
Far-sighted
Parallel light rays brought into focus at point BEHIND retina
Causes:
- Shorter axial length of globe
- Decreased refractive power of cornea, lens
Correction:
- Corrected by convex lens power
- Eye presented with converging rays
Ex: + 56.00 diopter eye corrected by +4.00 lens
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Astigmatism
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)
Correction:
- Combination of spherical and cylindrical lens power
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Presbyopia
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
Correction:
- 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
83
Accomodation
Ability of lens to change shape, become more convex
| - Increases refractive power
84
Aphakia
Absence of lens
- Eye is now short 20 diopters short of refracting power
Correction:
- 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)
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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
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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
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Age-related Macular Degeneration (ARMD)
Most common cause of blindness
Types:
1. Dry (non-neovascular)
2. Wet (neovascular)
Risk factors:
- Age
- Family History
- Hypertension
- Increased Cholesterol
- Smoking
Pathophys:
- 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
Histo:
- Deposition of eosinophilic material
- Thickening and fragmentation of Bruch’s membrane
- Degeneration of the RPE and loss of overlying photoreceptors
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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
Treatment:
- Vitamin combination with Zinc and Lutein slows progression approximately 25%.
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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)
Treatment:
- Laser photocoagulation of the CNVM (could worsen vision)
- Photodynamic Therapy (PDT)= Chemical injection followed by laser
- Inhibition of VEGF- YAY!
- Other
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Glaucoma
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
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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
Diagnosis:
- “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
Treatment:
- 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)
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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
Pathophys:
- The area between the iris and cornea suddenly closes, blocking drainage
- Short (hyperopic) “crowded” eye is a risk factor
Symptoms:
- 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
Treatment:
- 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
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Cataract
Reversible Opacification of lens
Risk factors:
- Age, Age, Age
- Heredity
- Trauma
- Steroid Use
- Certain Diseases: Diabetes, Retinitis Pigmentosa
Types:
- 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
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Causes of Refractive changes
Surface disease: dry eyes, epithelial defects
Cornea: dysfunction/ inflammation/ edema
Aqueous
- Inflammation- flare and cells= hypopion
- Blood= hyphema
Lens
- Cataract
- Lens dislocation (zonule fibers knocked out of place)
Vitreous
- Vitritis
- Hemorrhage
- Intravitreal foreign body
95
Circulatory emergencies in the eye
Arterial occlusions:
- Longstanding= vasculopathy
- Embolic: find origin
Venous occlusions:
- Manage systemic condition (HTN)
96
Retinal detachment
Neuro-sensory part of eye detaches from vasculature
- "Curtain dropping down"
- Must correct ASAP to prevent ischemia, central vision loss
97
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
98
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
99
Blunt trauma to the eye
```
Hyphema (blood in anterior chamber)
Traumatic iritis
Dislocated lens
Retinopathy
Ruptured globe
Orbital fracture
```
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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
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Hyphema
- can cause pupillary distortion (internal structure damage, ruptured globe)
- poor vision
- shield eye
- look for other blood problems (sickle cell)
Therapy:
- Topical steroids (reduce inflammation), but monitor IOP
- Cycloplegia (comfort, exam)
- Bed rest, upright to help RBCs settle (clot)
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Trauma to posterior segment of eye
Retinal edema--> hemorrhage--> macular edema
Choroidal rupture
Retinal tear, detachment
Traumatic optic neuropathy
Avulsion optic nerve
103
Chemical injury to eye
FLUSH
| Alkali damage--> whitened cornea due to vascular loss--> necrosis
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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)
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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
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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
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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
Exam:
- 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
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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
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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
110
Retinal folds
Circular/paramacular/perimacular:
- 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
111
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
112
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
Differential:
- 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
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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
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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
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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
116
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
```
```
Thrombocytopenia
Severe anemia
Fibrinogenemia
Leukemia
Hemophilia and factor deficiencies
Glutaric acidemia
Protein C deficiency
```
117
Findings in acute vs late abusive head trauma
Acute:
- hemorrhage: retina, vitreous
- circular retinal fold
- papilledema
- optic nerve avulsion= ripped out of back of eye
- Intracranial hemorrhage
Late:
- optic atrophy, cortical damage (long-term)
- retinal detachment
- retinoschisis
- vitreous opacity
- subretinal scar
- central visual impairment (cortical blindness)
- amblyopia
- myopia
118
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!
MOST VISION LOSS FROM CORTICAL DAMAGE OR OPTIC ATROPHY
