TOPNOTCH MEDICAL BOARD PREP OPHTHALMOLOGY SUPPLEMENT HANDOUT – Braylien W. Siy, MD-MBA & Timothy Joseph S.

Uy, MD-MBA
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OPHTHALMOLOGY SUPPLEMENT HANDOUT OUTLINE

II. Orbital Disorders VIII. Ocular Tumors
Dear Doctors,
III. Dry eye Disorders IX. Retinal Vascular Disorders
This supplement handout covers identified common eye disorders and basic knowledge relevant to IV. Conjunctival X. Acquired Macular Disorders
ophthalmology that a General Practitioner ought to know. Specific surgical techniques and guidelines are not Diseases XI. Retinal Detachment
sufficiently covered. Topics discussed are in no way exhaustive of all ophthalmologic conditions. Pharmacologic V. Disorders of the XII. Ocular & Orbital Trauma
therapies which have already been discussed in the TOPNOTCH Pharmacology review were no longer included
OUTLINE: Cornea XIII. Uveitis
here for brevity and omission of redundancy. This should serve as an adjunct to the Surgery
[Link] in the boards.
Disorders of the Lens
I. Disorders of the
Eyelids VII. Glaucoma
Good luck
- Len and TJ

REFERENCE: Riordan-Eva, Paul & john P. Whitcher. Vaughan & Asbury’s General Ophthalmology. 17th ed. McGraw-Hill. 2007.
DISEASE KEY FEATURES/PATHOPHYSIOLOGY SIGNS AND SYMPTOMS TREATMENT REMARKS
DISORDERS OF THE EYELIDS
Hordeolum - Melbomian gland involvement leads to an internal hordeoulum - Pain, redness and swelling of the - Warm compresses 3 to 4 times a day for 10-15
- Infection of Zeis’s or Moll’s glands are seen in smaller and more lids are the principal symptoms minutes; if the process does not begin to resolve
superficial external hordeolum within 48 hours, incision and drainage of the
- Most hordeola are caused by staphylococcal infections purulent material is indicated
Blepharoptosis - The upper lid normally rests approximately midway between the - Ptosis present in the primary - All types of ptosis are treated surgically with the
superior limbus and the pupillary margin. In ptosis, one or both upper position of gaze, with reduced exception of ptosis seen in Myasthenia gravis
eyelids assume an abnormally low position movement of the lid in upgaze and
- True congenital ptosis is seen in levator maldevelpment. In 25% of impaired closure on downgaze.
cases, the superior rectus muscle shares the same dystrophic
changes as the levator, resulting in weakness of upgaze
- Marcus Gunn syndome (jaw-winking phenomenon) – ptosis
decreases when the mandible is opened or is deviated to the
opposite side because the ptotic levator muscle is innervated by
motor branches of the trigeminal nerve as well as the occulomotor
nerve
Herpes Zoster - Common unilateral infection caused by varicella-zoster virus which - Pain in the distribution of the first - Oral Acyclovir 800mg five times daily for 7-10 days
Ophthalmicus typically affects the elderly and immunocompromised individuals division of the trigeminal nerve - Valacyclovir 1g TID, Famcyclovir 500mg TID and
- Initial maculopapular rash on the Vibudine 125mg OD
forehead progressing through - Topical acyclovir or pencyclovir cream, and a steroid-
vesicles and pustules to crusting antibiotic combination such as Fucidin-H can be used
- Periorbital edema may spread to TID until the crusts have separated
the other side, giving the
erroneous impression the the
condition is bilateral

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ORBITAL DISORDERS
Thyroid eye disease Thyroid ophthalmopathy involves an organ-specific autoimmune Five main clinical manifestation of Soft tissue Lubricants for superior limbic Once a patient
reaction in which a humoral agent (IgG antibody) produces: TED: involvement keratoconjunctivitis, corneal has Graves
(1) inflammation of extraocular muscles Soft tissue Photophobia, exposure and dryness; topical anti- disease, the
(2) inflammatory cellular infiltration involvement lacrimation, inflammatory agents major clinical
retrobulbar Lid Sequence of surgical procedures is risk factor for
discomfort retraction (1) orbital, (2) strabismus, (3) eyelid developing
Epibulbar • Mullerotomy, recession of thyroid eye
hyperemia the lower lid retractors, disease is
Lid Dalyrymple sign (lid botulinum toxin injection SMOKING
retraction retraction in Proptosis Systemic steroids, radiotherapy,
primary gaze) surgical decompression The upper lid
Kocher sign (staring Restrictive Surgical management IF diplopia in margin
and frightened myopathy the priamry or reading positions of normally rests
appreance of the gaze provided the disease is 2mm below the
eyes whic is quiescent and the angle of deviation limbus
particularly marked has been stable for at least 6 months
on attentive Optic Systemic steroids with orbital
fixation) neuropathy decompression
Von Graefe sign
(retarded descent
of the upper lid on
downgaze)
Proptosis Exposure
keratopathy,
corneal ulceration
and infection
Restrictive Opthalmoplegia
myopathy due to fibrosis of
recti muscles
Optic Impairment of
neuropathy central vision
Preseptal cellulitis - Infection of the subcutaneous tissues ANTERIOR to the orbital - Unilateral tender and red lid with - Oral Co-Amoxiclav 500/125mg every 8 hours
septum periorbital edema
- Chemosis is absent; visual acuity,
pupillary reactions and ocular
motility are NOT impaired

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Bacterial orbital - Life threatening infection of the soft tissues POSTERIOR to the orbital - Rapid onset of severe malaise, - IV cetazidime with oral metronidazole for anaerobic -
cellulitis septum fever, pain and visual impairment coverage
- Most common route is through an infection of the ethmoid sinus - Unilateral tender and warm red - Vancomycin is a useful alternative
periorbital edema + proptosis + - Regular monitoring of optic nerve function every 4
painful ophthalmoplegia + optic hours
nerve dysfunction

DRY EYE DISORDERS

Keratoconjunctivitis Any eye with some degree of dryness - Dryness, grittiness and burning - Dry eye is generally NOT curable and management is
sicca Non-Sjogren KCS Primary age-related hyposecretion sensation that characteristically structured around symptomatic control
Vitamin A deficiency worsens during the day - Tear substitutes, mucolytic agents, punctal
Evaporative KCS Meibomian gland dysfunction - Posterior blepharitis and occlusion, anti-inflammatory agents
Lagophthalmos meibomian gldn dysfunction - May develop peripheral superficial corneal
- Mild keratinization and hyperemia revascularization, epithelial breakdown, melting,
Sjogren syndrome Autoimmune inflammation and destruction of lacrimal and salivary of the conjunctiva perforation and bacterial keratitis
glands
CONJUNCTIVAL DISEASES
Acute Bacterial Most common isolates are S. pneumoniae, S. aureus, H. influenzae and - Acute onset of redness, grittiness, - Topical antibiotics (QID for up to 7 days). Ointments
Conjunctivitis Moraxella catarrhalis burning and discharge and gels provide a higher concentration of the drug
- Usually unilateral involvement for longer periods than drops.
Hyperacute Severe, profusely N. gonorrhea, N. - Discharge can initially be watery, o Chloramphenicol, aminoglycosides
(purulent) exudative form of kochii, N. mimicking viral conjunctivitis, but (gentamicin and neomycin), quinolones
bacterial conjunctivitis; delay in meningitidis rapidly becomes mucopurulent (ciprfloxacin, oflocaxin, levofloxacin,
conjunctivitis treatment may lead to - Superficial corneal punctate moxifloxacin), polymyxin B, fusidic acid and
severe corneal damage or epithelial erosions are common bacitracin
loss of the eye, septicemia - Systemic antibiotics are required in gonococcal and
or meningitis meningococcal conjunctivitis
Acute Often occurs in epidemics; Streptococcus
mucopurulent acute onset of conjunctival pneumoniae,
(catarrhal) hyperemia and moderate
conjunctivitis amount of mucopurlent
discharge
Subacute Thin, watery, flocculent H. influenza, E. Coli
conjunctivitis exudate
Chronic bacterial Occurs in px with Corynebacterium
conjunctivitis nasolacrimal duct diphtheriae,
obstruction, chronic S. pyogenes
dacrocystitis
Adult chlamydial - Oculogenital infection usually caused by serovars D-K of C. - Subacute onset of unilateral or Systemic therapy involves one of the following:
conjunctivitis trachomatis. Incubation period is about 1 week bilateral redness, lacrimation and 1. Azithromycin 1g repeated after 1 week is
watery/mucopurulent discharge generally the DOC
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- Large follicles are often most 2. Doxycycline 100mg BID for 10 days
prominent in the inferior fornix 3. Erythromycin, amoxicillin and ciprofloxacin
and may also involve the upper are alternatives
tarsal conjunctiva
- Superficial punctate keratitis is
common
- Peripheral subepithelial corneal
infiltrates may appear 2-3 weeks
after the onset of conjunctivitis
- Tender perauricular
lymphadenopathy

-
Trachoma - Leading cause of preventable irreversible blindness in the world Active Mixed SAFE strategy for trachoma management Superior limbal
- Recurrent infection elicits a chronic immune response consisting of trachoma follicular/papillary 1. Surgey for entropion and trichiasis, follicles may
cell-mediated delayed hypersensitivity (type IV) reaction to the conjunctivitis maintaning complete lid closure with resolve to leave
intermittent presence of chlamydial antigen and can lead to loss of associated with a bilamellar tarsal rotation a row of
sight. mucopurulent 2. Antibiotics shallow
discharge a. Single dose of azithromycin is DOC depressions
Cicatricial Linear or stellate to b. Erythromycin 500mg BID for 14 days (Herbert pits)
trachoma broad confluent 3. Facial cleanliness
conjunctival scars; 4. Environmental improvement
trichiasis, distichiasis,
corneal
vascularization and
cicatricial entropion

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Adenoviral Pharyngoconjunctival Fever of 38.3 – 40 C, sore Adenovirus - Eyelid edema and tender pre- Reduction of transmission risk by meticulous hand
conjunctivitis Fever throat, follicular Type 3, 4 auricular lymphadenopathy hygiene, avoiding eye rubbing and towel sharing
conjunctivitis in both eyes and 7 - Prominent conjunctival hyperemia Topical steroids may be required for severe
Transient superficial keratitis, and follicles membranous or pseudomembranous adenoviral
subepithelial opacities, - May be associated with conjunctivitis
nontender preauricular conjunctival hemorrhages,
lymphadenopathy chemosis, membranes and
Epidemic Usually bilateral Adenovirus pseuodmembrane formation
Keratoconjunctivitis Conjunctival injection, types 8, - Epithelial microcysts are common
moderate pain and tearing 19, 29, and during the early stage while
followed in 5-14 days by 47 punctate epithelial keratitis may
photophobia, epithelial develop within 7-10 days of the
keratitis, & round onset of symptoms
subepithelial opacities
Edema of the eyelids,
chemosis and conjunctival
hyperemia mark the acute
phase
Pingueculum - Extremely common, innocuous, usually bilateral and asymptomatic - Yellow-white mound or - Treatment usually unnecessary - Most
‘elastotic’ degeneration of the collagen fibers of conjunctival strioma aggregation of smaller mounds on usually
the bulbar conjunctiva adjacent to located in
the limbus the naso-
temporal
limbus
Pterygium - Triangular fibrovascular subepithelial ingrowth of degenerative - Irritation and grittines may be - Medical treatment of symptomatic patients involves
bulbar conjunctival tissue over the limbus onto the cornea caused by a dellen effect at the tear substitutes, and topical steroids for
advancing edge due to inflammation
interference with the precorneal - Surgical management leads to definitive result
tear film
DISORDERS OF THE CORNEA
Bacterial keratitis - Pseudomonas aeruginosa is a ubiquitous gram-negative bacillus that Eye pain, photophobia, blurred vision - Topical therapy can achieve high tissue
is typically aggressive and is responsible for over 60% of contact lens and mucopurulent/purulent discharge concentration and initially should consist of broad
related keratitis (1) Epithelial defect associated spectrum antibiotics which cover most common
with a larger infiltrate pathogens
Streptococcus pneumoniae Gray, fairly well circumscribed (2) Enlargement of the infiltrate
ulcer that spreads erratically and defect - Mydriatics (cyclopentolate, homatropine or
from the original site of (3) Stromal edema, folds in atropine) are used to prevent the formation of
infection toward the center Descemet membrane and posterior synechiae and to reduce pain
of the cornea anterior uveitis
Pseudomonas aeruginosa Ulcer begins as a gray or (4) Chemosis and eyelid Empirical Fluoroquinolone OR Cefuroxime
yellow infiltrate at the site of swelling treatment + Gentamycin
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a break in the corneal (5) Rapid progression of Gram + cocci Cefuroxime OR Vancomycin or
epithelium. Infiltrate and infilitration with an Teicoplanin
exudate may have a bluish enlarging hypopyon Gram – rods Gentamycin OR
green color (6) Scarring, vascularization and Fluoroquinolone OR
Staphylococcal ulcers Indolent ulcers associated opacification Ceftazidime
with hypopyon and some Gram – cocci Fluoroquinolone OR Ceftriaxone
surrounding corneal Mycobacteria Amikacin OR clarithromycin
infiltration; often superficial Nocardia Amikacin OR TMP-SMX
Fungal keratitis - Yeasts (e.g. genus Candida) are responsible for most cases of fungal - Gradual onset of pain, grittiness, Removal of the epithelium over the lesion may enhance
keratitis in temperate climates photophobia, blurred vision and penetration of antifungal agents. Regular mucus and
- Filamentous fungi (e.g. genera Fusarium and Aspergillus) are watery OR mucopurulent necrotic tissue removal may be helpful
reponsible for most cases in tropical climates discharge Topical treatment should be given hourly for 48 hours
Candida Amphotericin B,
Econazole,
Natamycin,
Fluconazole,
Clotrimazole
Filamentous infection Natamycin,
Econazole
DISORDERS OF THE LENS
Cataracts - Any opacity in the lens; aging is the most common cause of cataract. - Most cataracts are not visible to - Visual improvement is the most common indication
- Cataractous lenses are characterized by protein aggregates that the casual observer until they for cataract surgery
scatter light rays and reduce transparency. Factors thought to become dense enough to cause - Phacoemulsification has become the preferred
contribute to cataract formation include oxidative damage (from free severe vision loss method of cataract extraction over the last 15 years
radical reactions), UV damage and malnutrition
- Clinical degree of cataract
Mature cataract Lens protein is opaque formation is judged primarily by
Immature cataract Transparent protein the Snellen visual acuity test. The
Hypermature Liquefaction of cortical proteins decrease in VA is directly
cataract proportionate to the density of the
Morgagnian cataract Hypermature cataract when the lens cataract
nucleus floats freely in the capsular bag

GLAUCOMA
Glaucoma - Potentially progressive and characteristic optic neuropathy which is
associated with visual field loss and in which intraocular pressure is
usually a key modifying factor
- In the general population, the mean IOP is 16mmHg
Primary open angle - Generally bilateral disease of adult onset characterized by an IOP >21 - Visual symptoms are usually - Primary aim of treatment is to prevent functional
glacuoma mmHg, glaucomatous optic nerve damage, an open anterior chamber absent unless damage is advanced impairment of vision within the patient’s lifetime by
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angle, characteristic visual field loss with progression of damage slowing the rate of ganglion cell loss. Currently, the
- Retinal ganglion cell death occurs predominantly through apoptosis only proven method is the lowering of IOP
rather than necrosis. Direct mechanical damage to retinal nerve
fibers at the optic nerve head as they pass through the lamina
cribrosa AND ischemic damage due to compression of blood vessels
supplying the optic nerve head are implicated
Normal pressure - IOP is consistently equal to or less than 21 mmHg, signs of optic
glaucoma nerve damage in a characteristic glaucomatous pattern, an open
anterior chamber angle, visual field loss as damage progresses
Primary angle Occlusion of the trabecular meshwork by the peripheral iris Acute Congestive Angle Closure Initial Treatment
closure glaucoma (iridotrabecular contact) obstructing aqueous outflow • Visual acuity is usually 6/60- • Assume a supine position to encourage the
HM lens to shift posteriorly under the influence of
Primary angle Gonioscopy shows posterior meshwork ITC in • IOP is usually very high (50- gravity
closure susoect 3 or more quadrants but no PAS 100 mmHg) • Acetazolamide 500mg given IV if IOP
Normal IOP, optic disc and visual field • Conjunctival hyperemia with >50mmHg and orally if IOP is <50 mmHg
Primary angle Gonioscopy shows 3 or more quadrants of violaceous circumcorneal • Topical apraclonidine 1%, timolol 0.5%,
closure ITC with raised IOP and/or PAS. injection prednisolone 1% or dexamethasone 0.1% to
Normal optic disc and field • Shallow anterior chamber the affected eye
Primary angle Gonioscopy shows ITC in 3 or more quadrants and aqueous flare may be • Pilocarpine 2-4% one drop to the affected eye,
closure glaucoma Optic neuropathy present repeated after half an hour, and one drop of
1% as prophylaxis into the other eye
Subsequent medical treatment
• Pilocarpine 2% QID to affected eye and 1%
QID to the other eye
• Topical steroid (prednisolone 1% or
dexamethasone 0.1%) QID if the eye is acutely
inflamed

OCULAR TUMORS
Retinoblastoma Most common primary intraocular malignancy of childhood Usually presents within the first year Tumors of no more than 3 mm diameter and 2mm
Tumor is composed of small basophilic cells with large hyperchromatic of life in bilateral cases and around 2 thickness
nuclei and scanty cytoplasm years of age if the tumor is unilateral • Photocoagulation, cryotherapy and
1. Flexner-Wintersteiner rosettes • Leukocoria is the most chemotherapy
2. Homer-Wright risettes (pseudorosettes) common presentation Tumors up to 12mm wide and 6mm thiks
3. Fleurettes • Strabismus is the second • Bracchytherapy, primary chemotherapy with I
most common carboplatin etoposide and vincristine given in
3 to 6 cycles; external beam radiotherapy
Large tumors
• Chemotherapy to achieve chemoreduction
• Enucleation if there is rubeosis, vitreous
hemorrhage or optic nerve invasion
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RETINAL VASCULAR DISORDERS

Diabetic Duration of diabetes is the most important risk factor. Clinically significant macular edema:
retinopathy Predominantly a microangiopathy in which small blood vessels are  Retinal thickening within 500um of
particularly vulnerable to damage from hyperglycemia the centre of the macula
1. Intracellular sorbitol accumulation, oxidative stress due to free  Exudates within 500 um of the MAINSTAY: good control of hyperglycemia, systemic
radical excess, and accumulation of advanced glycation end centre of the macular, if associated hypertension and hypercholesterolemia
product with retinal thickening
2. Capillaropathy characterized by death of pericytes, thickening  Retinal thickening one disc area Pan-retinal Laser Photocoaculation (PRP) reduces the
of capillary BM, loss of vascular smooth muscle cells and (1500 um) or larger, any part of incidence of severe visual loss from proliferative
proliferation of endothelial cells which is within one disc diameter diabetic retinopathy by 50% with induction of
3. Neovascularization caused by capillary non-perfusion leading of the centre of the macula regression of new vessels
to retinal hypoxia

Nonproliferative Very mild: microaneurysms only

Retinoipathy Mild: any or all of: microaneurysms, retinal
hemorrhages, exudates cotton wool spots
Moderate: severe retinal hemorrhages in 1-3
quadrants or mild intraretinal microvascular
abnormalities (IRMA); significant venous beading
present in no more than 1 quadrant
Severe: hemorrhages in all 4 quadrants,
significant venous beading in 2 or more udrants,
moderate IRMA in 1 or more quadrants
Very severe: 2 or more criteria for severe PDR
Maculopathy Focal or diffuse retinal thickening or edema
which allows leakage of fluid and plasma
constituents into the surrounding retina

Retinal thickening within 500 microns of the

fovea, hard exudates within 500 micorns of the
fovea associated with retinal thickening or retinal
thickening greater than one disc diameter in size
Proliferative Presence of any new vessels on the optic disc or
Retinopathy elsewhere in the retina.
Branch Retinal Vein - Arteriosclerosis is an important causative factor for branch RVO. - Presentation depends on the extent of macular circulation compromised by the occlusion. Site of
Occlusion Because a retinal arteriole and its corresponding vein share a - If with macular involvement, often present with sudden onset of blurred vision and occlusion is
common adventitial sheath, thickening of the arteriole appears to metamorphopsia, or a relative visual field defect often
compress the vein. This causes secondary changes, including venous - Dilatation and tortuosity of the affected venous segment identifiable as
endothelial cell loss, thrombus formation and potential occlusion - Flame-shaped and dot/blot hemorrhages, retinal edema, cotton wool spots affecting the an
sector of the retina drained by the obstructed vein arteriovenous
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- Age is the most important factor - FA would show variable delayed venous filling, blockage by blood, staining of the vessel wall, crossing point
- Chronic macular edema is the most common cause of persistent poor hypofluorscence due to capillary non-perfusion
visual acuity after BRVO
Treatment of associated macular edema
1. Grid laser photocoagulation
2. Intravitreal triamcinolone
3. Periocular steroid
4. Intravitreal anti-VEGF agents
5. Arteriovenous sheathotomy
Ischemic central - Rapid onset venous obstruction resulting in decreased retinal - Sudden and severe visual - Prognosis is extremely poor due to macular ischemia
retinal vein perfusion, capillary closure and retinal hypoxia impairment
occlusion - Profound vascular leakage, rubeosis iridis and raised IOP - Marked relative afferent pupillary
defect
- Severe tortuosity and
engorgement of all branches of the
central retinal vein, extensive deep
blot and flame shaped
hemorrhages involving the
peripheral retina and posterior
pole, severe disc edema and
hyperemia
Branch retinal - Sudden and profound painless
artery occlusion altitudinal or sectoral visual field
loss
- Narrowing (attenuation) of
arteries and veins with sludging
and segmentation of the blood
column
Central retinal Sudden and profound loss of vision Retinal artery occlusion is an emergency because it
artery occlusion - VA is severely reduced. No causes irreversible visual loss unless the retinal
perception of light usually circulation is re-established prior to the development of
indicates opthalmic artery retinal infarction
occlusion affecting both the retinal 1. Supine position to improve ocular perfusion
and choroidal circulartion 2. Ocular massage
- The orange reflex from the intact 3. Anterior chamber paracentesis
choroid stands out at the thin 4. Topical apraclonidine, timolol and IV
foveola, in contrast to the acetazolamide
surrounding pale retina, giving rise 5. Sublingual isosorbide dinitrate
to the ‘cherry-red spot’ 6. Breathing a high oxygen and carbon dioxide
appearance mixture for possible dual effect of retarding
ischemia and vasodilation

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7. Hyperosmotic agents
8. Transluminal Nd-YAG laser embolysis
9. Thrombolysis
ACQUIRED MACULAR DISORDERS
Age-Related - Leading cause of IRREVERSIBLE blindness in the developed world - Gradual impairment of vision over 1. Oral vitamins and antioxidants comprising Vitamin Drusen:
Macular months or years; both eyes are c (500mg), Vitamin E (400 IU), betacarotene extracellular
Degeneration - Pathogenesis is still poorly understood however, degeneration of the usually affected but often (15mg) and zinc (80mg) and copper (2mg) daily deposits
RPE linked to oxidative stress seems to be a crucial component. asymmetrically reduces the 5-year risk of progression to late located at the
Progressive diffuse thickening of Bruch’s membrane reduces the ARMD from 28% to 20% in patients. interface
ability of oxygen to diffuse through to the RPE 2. Smoking is a proven risk factor for development of between the
all forms of macular degeneration RPE and Bruch
Early Limited drusen, pigmentary change or retinal pigment 3. Retinal laser photocoagulation reduces the extent membrane
ARMD epithelial atrophy of drusen but increases the rate of choroidal
Late GA (dry-variant): well demaracated areas, larger than two neovascularization
ARMD disc diameters, of atrophy of the RPE and photoreceptor 4. Photodynamic therapy involves IV infusion of a
cells photosensitivie dye that preferentiialy accumulates
Neovascular (wet-variant): (+) choroidal in active new levels and then activated by a low-
neovascularization or serous retinal pigment epithelial energy visible laser. This produces localized
detachment thrombosis of the new vessels.
5. Anti-VEGF therapy (Ranibizumab, Bevacizumab)
works under the premise of blockade of expansion
of choroidal neovascular membrane
RETINAL DETACHMENT
Rhegmatogenous - Most common type characterized by full thickness break in the - The classic premonitory symptoms 1. Pneumatic retinopexy – air or expandable gas is
retinal detachment sensory retina, variable degrees of vitreous traction and passage of reported in ~60% of patients with injected into the vitreous to maintain the retina in
liquefied vitreous through the break into the subretinal space spontaneous rhegmatogenous RD position, while chorioretinal adhesion is induced by
- are flashing lights and vitreous laser or cryotherapy
- Usually preceded by a posterior vitreous detachment and is floaters 2. Scleral buckling – maintains retina in position while
associated with myopia, aphakia, lattice degeneration, and ocular - A visual field defect is perceived as chorioretinal adhesion forms, by indenting the
trauma a black curtain. A lower field sclera with a sutured explant in the region of the
o Horeshoe tears are most common in superotemporal defect is usually appreciated more retinal break. Relieves vitreoretinal traction and
quadrant quickly by the patient than an displaces subretinal fluid. Success rate is 92-94%
o Atrophic holes in the temporal quadrants upper field defect 3. Pars Plana vitrectomy – relief of vitreoretinal
o Retinal dialysis in the inferotemporal quadrant - Marcus Gunn pupil is present in an traction, internal drainage of subretinal fluid if
eye with an extensive RD necessary by infection of perfluorocarbons or
irrespective of type heavy liquids, and injection of air or expandable
- IOP is usually lower by ~ 5mmHg gas to maintain the retina in position, or injection
with the normal eye of oil if longer-term tamponade or the retina is
- Mild iritis is common required.
Traction Retinal - Most commonly due to proliferative diabetic retinopathy - Photopsia and floaters are usually - Pars plana vitrectomy, gas tamponade, silicone oil or
Detachment - Traction is due to formation of vitreal, epiretinal or subretinal ABSENT scleral buckling may be used
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membranes consisting of fibroblasts and glial and retinal pigment - Visual field defect usually -
cells progresses slowly and may
- Has a more concave surface and is likely to be more localized, usually become stationary for months or
not extending to the ora serrata years
Exudative Retinal - Occurs in the ABSENCE of either retinal breaks or vitreoretinal - Photopsia is absent because there - Treatment depends on the cause; most cases
Detachment traction is no vitreoretinal traction resolve spontaneously while others are treated with
(Serous OR - Result of the accumulation of fluid beneath the sensory retina and although floaters may be present systemic corticosteroids
Hemorrhagic) are caused primarily by diseases of the retinal pigment epithelium
and choroid
OCULAR & ORBITAL TRAUMA
Blow out orbital Caused by sudden increase in the orbital pressure by an impacting object - Periocular signs include variable Indications for surgical repair of blowout orbital
floor fracture which is greater in diameter than the orbital aperture ecchymosis, edema and fractures:
subcutaneous emphysema • Persistent diplopia within 30 degress of primary
• Le Fort I is below the orbital floor, II passes through the nasal and - Infraorbital nerve anesthesia position of gaze with evidence of soft tissue
lacrimal bones in addition to the maxilla forming the medial orbital involving the lower lid, cheek, side entrapment
floor, III involves the medial and lateral walls and the orbital floor in of nose, upper lip, upper teeth and • Large fracture (half the orbital floor) which is likely
the presence of separation of the facial skeleton from the cranium gums is very common due to to cause late enophthalmos
• Optic neuropathy may be due to direct injury from a fragment of fracture involving the infraorbital
bone, usually due to ethmoid sinus fracture with or without canal
involvement of the optic canal or due to indirect injury from - Diplopia
transmission of forces to the optic canal - Enophthalmos
• Carotid artery cavernous sinus fistulas are associated with orbital
apex fractures, and the orbit should be auscultated for bruits
Chemical injuries Alkalis tend to penetrate more deeply than acids, as the latter coagulate Copious irrigation is crucial to minimize duration of
surface proteins, forming a protective barrier. contact with the chemical and normalize the pH in the
1. Necrosis of the conjucntival and corneal epithelium with disruption Grade Clear cornea (epithelial conjunctival sac as soon as possible
and occlusion of the limbal vasculature 1 damage only) and no - Sterile normal saline or Ringer lactate should be
2. Deeper penetration causes the breakdown and precipitation of limbal ischemia used to irrigate the eye for 15-30 minutes or until
glycosaminoglycans and stromal corneal opacification Grade Hazy cornea but with pH is neutral
3. Anterior chamber penetration results in iris and lens damage 2 visible iris details and less - Topical anesthetic should be instilled prior to
than one-third of the irrigation
libus being ischemic Double eversion of the upper eyelid should be
Grade Total loss of corneal performed to remove any retained particulate matter
3 epithelium, stromal haze Debridement of necrotic areas of corneal epithelium
obscuring iris-details and
between one-third and
half limbal ischemia
Grade Opaque cornea and more
4 than half limbal ischemia
UVEITIS
Acute Anterior Most common form of uveitis, of sudden onset and a duration of 3 Sudden onset of unilateral pain, Corticosteroids and cycloplegic/mydriatic agents are the

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Uveitis months or less photophobia and redness which may mainstays of therapy for uveitis. Care should be taken
Keratic precipitates may be large ("mutton fat," or "granulomatous"), be associated with lacrimation. to rule out an epithelial defect and ruptured globe when
small (nongranulomatous), or stellate VA is good at presentation a history of trauma is elicited and to check corneal
Chronic Anterior Persistent inflammation that promptly relapses, in less than 3 months, Patients are usually asymptomatic sensation and intraocular pressure to rule out herpes
Uveitis after discontinuation of treatment. Inflammation may be granulomatous until the development of cataracts or simplex or herpes zoster infection. Aggressive topical
or non-granulomatous. Bilateral involvement is more common than in band keratopathy therapy with 1% prednisolone acetate, one or two
AAU drops in the affected eye every 1 or 2 hours while
Posterior Uveitis Encompasses retinitis, choroiditis and retinal vasculitis awake, usually provides good control of anterior
• Retinitis: retinal opacities with indistinct borders due to inflammation. Prednisolone acetate is a suspension and
surrounding edema needs to be shaken 30 to 40 times prior to each use.
• Choroiditis: round, yellow nodule Homatropine, 2–5%, used two to four times daily, helps
• Vasculitis: yellowish or grey-white, patchy perivascular cuffing prevent synechia formation and reduces discomfort
that may be associated with hemorrhage. from ciliary spasm.
Sarcoidosis uveitis T-lymphocyte mediated noncaseating granulomatous inflammatory Heerfordt syndrome (uveoparotid
disorder of unknown cause fever) is characterized by uveitis,
parotitis, fever and cranial nerve
palsy, usually the seventh nerve.

CORNEAL TRANSPLANTATION (Keratoplasty)

Initial Examination of Ocular Trauma 1. Penetrating Keratoplasty (PK): full thickness corneal replacement
1. History should include estimate of VA prior to and immediately following injury 2. Lamellar Keratoplasty -partial thickness corneal replacement with a variable amount of stroma
a. Note whether visual loss was slowly progressive or sudden in onset a. Deep Lamellar keratopasty – almost all of the cornea EXCEPT the endothelium is replaced
2. If visual loss is sever, check for light projection, two-point discrimination and the presence of b. Deep Lamellar Endothelial keratoplasty – endothelium with only a thin layer of stroma is
an afferent pupillary defect transplanted
3. Test ocular motility and periorbital skin sensation, palpate for defects in the bony orbital rim
4. Corneal surface is examined for foreign bodies, wounds and abrasions Procedures for corneal harvesting and transplantation
5. Bulbar conjunctiva is inspected for hemorrhage, foreign material or lacerations 1. Enucleation should be done soon after death and refrigerated immediately. Whole eyes should be
6. Depth and clarity of the anterior chamber are noted used within 48 hours.
7. Bilateral size, shape and light reaction of the pupils should be compared 2. Corneoscleral caps stored in nutrient media may be used up to 6 days after donor death.
Immediate Management of Ocular Trauma 3. Preservation in tissue culture media allows storage for as long as 6 weeks.
1. If there is obvious rupture of the globe, avoid further manipulation until surgical repair under 4. For lamellar and deep lamellar keratoplasty, corneas CAN be frozen, dehydrated or refrigerated for
sterile conditions can be undertaken several weeks since the endothelial cells are not as important in these procedures.
2. No cycloplegic agents or topical antibiotics should be instilled prior to surgery because of
potential toxicity LASIK surgery
3. Analgesics, antiemetics and tetanus antitioxin are given as needed • Cuts a thin lamellar corneal disk which is folded back. Laser of the stromal bed produces the desired
4. Induction of GA should NOT include the use of depolarizing neuromuscular blocking agents carefully programmed reshaping of the cornea and the flap is repositioned
since these transiently increase pressure on the globe thus increasing tendency to herniation 1. Photorefractive keratectomy (PRK) – only the corneal epithelium is removed prior to laser
of intraocular contents treatment
2. Laser epithelial keratectomy (LASEK) – the epithelium is removed with dilute alcohol and
replaced after laser treatment
TOPNOTCH MEDICAL BOARD PREP OPHTHALMOLOGY SUPPLEMENT HANDOUT 3. Epi-LASIK – the epithelium is removed with a microkeratome and replaced after laser treatment.
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