Ophthalmology-OSCE Reviewer

07 OPHTHALMOLOGY
PART A. Basic Eye Exam- VAGETF
VISUAL ACUITY GROSS EXAM EXTRAOCULAR MUSCLES TONOMETRY FUNDOSCOPY

 Always start with vision  Observe the following  Face the patient at equal eye  Palpation tonometry to assess  Steps
(baseline)  Suggestion is to do it from level intraocular pressure  Ensure patient is
 General instructions most external to internal so it  Instruct to follow the tip of your  DO NOT do if globe rupture is comfortable
 Start with right eye (as is systematic index finger using just the eyes suspected  Dim the room (to dilate
standard)  Alignment  Move in a “H” position  Steps pupils)
 Ask patient not to squint  Via the corneal light reflex  Check EOMs one eye at a time  Ask the patient to look down  Ask the patient to fixate at a
 Watch out for memorizers  Eyebrows, lids, and lashes (duction), then together (without closing eyes) distant object
 Lateral eyebrow sparseness (version)  Place both index fingers on  Use R hand to hold
 Queen Anne’s sign  Recording the right upper lid ophthalmoscope and view
Distance Vision  Hypothyroidism  Draw an asterisk (see Figure  Press gently using one finger the R eye then vice versa
 Test using Snellen Chart  Bulbar and palpebral 7-1) while the other assesses  Begin 8-10 inches away,
 20 ft or 6 m away conjunctiva  ARrows for Right eye rebound slightly on the lateral side
 Steps  Hyperemic, pale?  CircLes for Left eye  Repeat for left eye  Find the ROR
 Uncorrected  Sclera  See Figure 7-2  Move closer (while keeping
 Corrected  Icteric vs non-icteric?  Recording the ROR in view) coming
 Pinhole (w/ or w/o glasses)  Cornea  Soft (normal), firm, hard, from 30-45 degrees
 Recording  Clear, hazy, lesions? hypotonic? temporally
 Pupils  Look for a blood vessel then
 Shorthand
 Round, equal, reactive? follow it until you see the
 OD – right eye
 Anterior chamber disc
 OS – left eye
 Shine a light tangentially from  Note your findings
 OU – both eyes
 Recording (normal, OU)
 Usually use fractions the temporal area to assess
 20/200 (patient/normal) depth of anterior chamber  (+) ROR
 What the patient can read  Clear media
at 20 ft can be read by a  Distinct disc borders
Figure 7-1. EOM Notation  Cup:disc ratio 0.3
normal person at 200 ft Figure 7-2. Palpation Tonometry
Near Vision  Arterovenous ratio 2:3
 Test using Jaeger Chart  (+) Foveal reflex
 For 35 years and above to  (-) hemorrhages, exudates,
screen for presbyopia other lesions
 Steps (one eye at a time)  See Figure 7-3 for a normal
 Uncorrected fundoscopy finding
 Corrected
 Normal is J1+
YL7: 07.01 OSCE Reviewer: Ophthalmology Module | Gio de la Cruz, Melina Barzaga, Elysse Salindo, Camille Sison, Jose Ma. Zaldarriaga 1 of 27
Figure 7-3. Normal Fundoscopy Findings, Right Eye Figure 7-4. Example Recording of Basic Eye Exam Findings
PART B. Common Eye Diseases
*Disclaimer: This section does not cover ALL of the diseases/conditions discussed/mentioned in the module. Only those that are most common, extensively discussed, and
highlighted are presented below.
CLINICAL MANIFESTATIONS & COURSE PATHOGENESIS DIAGNOSIS TREATMENT

Age-related Cataract
 Quick review: Anatomy of the Lens  Classification:  Slit lamp biomicroscopy  Surgical extraction- only definite
treatment
1. Subcapsular  majority of current cataract
 May be anterior or posterior surgery carried out through
 Glare: most common clinical Phacoemulsification
Aqueous
presentation
 More problems with reading than with 1. Capsulorrhexis-removing the
distance vision anterior capsule via shear and stretch
forces
2. Nuclear Iris
Cornea Lens
 Central darkening of the lens 2. Hydrodissection- separating the
 May cause an increase in myopia nucleus and cortex of the lens from the
 Distance vision is usually more posterior capsule
affected than near.
3. Removal of nucleus- nucleus is
3Cortical broken up into “fragments” using an
 Spoke-like opacities Fig.7-6. Normal anterior chamber via slit lamp ultrasonic probe; each fragment is
emulsified and aspirated
4. Cortical clean-up
Fig.7-5. Normal anatomy of the lens
5. Insertion of the intra-ocular lens
(IOL)
6. Completion- aspiration of remaining

debris, sealing of side port incisions,
subconjunctival injection of steroid and
antibiotic
 Other surgical methods of

cataract extraction
 Extracapsular extraction
 Intracapsular exctraction
Fig.7-7. Posterior subcapsular cataract  Couching
 Overview of Age-related Cataract  Cataract Maturity

 Opacity of the natural crystalline lens
 Most common cause of vision loss in 1. Immature lens is just partially opaque
people over age 40 y.o.
 Can be distinguished into several subtypes, 2. Mature lens is completely opaque
but they usually look the same “cloudy or
white pupil” on just gross examination
 Complications of Age-related Cataract

 posterior lens capsular opacification
occurring in 20% of cases
 acute or chronic bacterial endophthalmitis
 retinal detachment especially for myopes
Fig.7-8. Nuclear cataract
Fig.7-9 Immature vs mature cataract
3. Hypermature lens- shrunken and wrinkled

anterior chamber; “hinog na”
Fig7-10. Hypermature cataract Fig.7-11. Cortical cataract
Acute angle-closure glaucoma

*Note: There are many other subtypes of  Pathogenesis  Gonioscopy  Systemic carbonic anhydrase
glaucoma but AAG is the one extensively  elevation of intraocular pressure as a  Very shallow anterior chamber inhibitors
discussed in class. Other types of glaucoma: result of obstruction of the anterior  Topical beta blockers
Chronic open-angle glaucoma, development chamber angle by the peripheral iris  Miotics, alpha agonists, and steroids
glaucomas, neovascular glaucoma  Laser peripheral iridotomy once
 Risk Factors the cornea has cleared after the
 SSx  increasing age (over 60 y.o.; because of administration of these medications.
 IOP: 50-100 mmHg (Normal: 11-21 mmHg) the normal increase in the size of the
 Circumcorneal (ciliary) injection lens with ageing)
 Edematous, “steamy” cornea  female sex
 Fixed, mid-dilated, oval pupil  anatomically predisposed eye
(hypermetropia, shallow anterior
chamber, narrow angle)
Fig.7-13 Normal anterior chamber angle via

gonioscopy
Fig.7-17. Post-laser iridotomy
Fig.7-14. AAG with ciliary injection, mid-dilated

pupil, edematous steamy cornea
Fig.7.16. Narrow anterior chamber angle via
gonioscopy
Fig.7-15. AAG with a more pronounced steamy
cornea
Acute Anterior Uveitis (AAU)

• Quick review: What is the Uveal Tract? • Causes  Slit lamp biomicroscopy will reveal the  topical steroids and mydriatics:
following characteristic findings mainstay of treatment
 Layer of tissue between the outer later  commonly idiopathic
 Endothelial cellular dusting  periocular steroid injection
(cornea and sclera) and inner layer (retina) of  HLA-B27-associated: ankylosing
 Cells and flare  systemic steroids,
the eye spondylitis, Reiter’s syndrome, psoriatic
 Composed of THREE structures: Iris,  Posterior synechiae (adhesion of the iris immunosuppressive agents,
arthritis
to the lens), may be visible even grossly. antibiotics if etiology is infectious
Ciliary Body, Choroid  Infections: Herpes zoster and simplex,
syphilis, TB
 Inflammatory Bowel Disease
• Overview of AAU  Juvenile Idiopathic Arthritis
 may either be iritis (inflammation of the iris)  Non-infectious systemic diseases:
or iridocyclitis (inflammation of the iris and Sarcoidosis, Behçet’s disease, Vogt-
ciliary body) Koyanagi-Harada (VKH) syndrome
• SSx
 sudden onset of unilateral photophobia,
redness, pain, and blurring of vision
 ciliary injection
 How to distinguish from AAG? No steamy
cornea, no fixed mid-dilated pupil in Fig.7-18. Endothelial dusting
uveitis
Fig.1. Posterior synechiae
Fig.7-19. AA Uveitis, gross
Fig.7-20. Cells and Flare
Diabetic Retinopathy (DR)

 Most common cause of irreversible blindness in  Primary cause: chronic hyperglycemia  Screening  Prevention of Progression
middle-aged subjects (working age)  Capillary pericyte cell loss  endothelial  Type 1 Diabetes: First examination 3-5  Good control of hyperglycemia,
 Risk factors years after diagnosis of diabetes, systemic hypertension, and
 Chronic hyperglycemia cell loss  microaneurysm formation  recommended yearly follow up hypercholesterolemia
 Hypertension leakage, hemorrhage  hypoxia   Type 2 Diabetes: First examination at  Treatment: Nonproliferative DR
 Hypercholesterolemia neovascularization  hemorrhage,
the time of diagnosis of diabetes,  Mild and moderate
 Smoking fibrosis, traction
recommended yearly follow-up nonproliferative diabetic
 Type I (insulin-dependent) diabetics: do not retinopathy are generally not
develop retinopathy for at least 3-5 years after  Monitoring treated
onset of the systemic disease  Frequency of monitoring depends on  When clinically significant ME is
 Type II (non-insulin-dependent) diabetics: may severity present, intravitreal antivascular
have retinopathy at the time of diagnosis, and it  Frequency ranges between every 2-12 endothelial growth factor (VEGF)
may be the presenting manifestation months or laser treatment (focal
photocoagulation) are initial
Stages of DR treatment options
1. Nonproliferative Diabetic Retinopathy (milder  Treatment: Proliferative DR
stage)  Panretinal photocoagulation
 Microaneurysms and hemorrhages, hard (PRP)
exudates, and cotton-wool spots  Vitrectomy
 Venous abnormalities (beading, loops),  Anti-VEGFs
intraretinal microvascular abnormalities
(IRMA), increased hemorrhage, and
exudation
Fig. 7-20 Color fundus photograph of nonproliferative

diabetic retinopathy showing retinal hemorrhages, yellow
lipid exudates, and dull white cotton wool spots (nerve
fiber layer infarcts). (UpToDate, 2016)
2. Proliferative Diabetic Retinopathy

 Neovascularization (more friable vessels
that tend to bleed easily), vitreous
hemorrhage, and traction retinal detachment
 Hallmark: Neovascularization Which can lead
to leakage
Fig 7-21 Color fundus photograph of proliferative diabetic

retinopathy displaying prominent neovascularization at
the disc (NVD). (UpToDate, 2016)
Fig 7-23 Color fundus photograph displaying vitreous
hemorrhage arising from neovascularization at the disc
(NVD). (UpToDate, 2016)
3. Diabetic Macular Edema (ME)

 Hard exudates, retinal thickening
 Swelling at the central portion
Fig 7-24. (A) Optical coherence tomography (OCT) of

diabetic macular edema. There are numerous large cysts
visible within the macula (arrows), and the retinal
thickness is increased.
(B) OCT of normal macula (for comparison) showing
typical foveal contour. (UpToDate, 2016)
Age-related Macular Degeneration (AMD)
 A degenerative disease of the central portion of  Pathogenesis is still poorly understood;  Amsler Grid  Prevention
the retina (the macula) that results primarily in however, degeneration of the retinal  Distortion is a symptom of exudation  Persons older than 55 years
loss of central vision pigment epithelium, linked to oxidative  Fluid distorts it should have dilated eye
 Leading cause of irreversible blindness in the stress, seems to be a crucial component  Suggests that there is some kind of examinations to determine their
developed world  An insult to the normal mechanism of neovascularization or inflammation risk of developing advanced AMD
 Genetic susceptibility involving the clearing cellular debris or waste through in the back of the eye  Those with the following should
complement pathway and environmental risk the RPE and phagocytes  Helps distinguish between dry and consider taking a supplement of
factors, including increasing age, white race,  Debris accumulates in the inner wet AMD antioxidants plus zinc:
and smoking collagenous layer of Bruch’s  Fluorescein angiography  Extensive intermediate size
membrane  Definitive diagnostic exam drusen  
 Retinal pigment attachments/junk, or  Detects wet AMD  At least 1 large drusen  
Classification drusen, develops because the junk is  Dye is injected and then pictures are  Non-central geographic atrophy
1. Dry AMD – Geographic atrophy not cleared away taken of the fluoresced vessels in 1 or both eyes, or  
 The photoreceptors deteriorate, retinal  Large, soft  Abnormal vessels can be seen in wet  Advanced AMD or vision loss
pigment epithelium atrophies  Yellow waste deposits that are stored AMD due to AMD in 1 eye 
 They will never lose all of their vision in between the RPE and Bruch’s  It is expensive and patients can  AND without contraindications
 Patient will lose central vision but retain membrane experience allergic reaction from the dye such as smoking
peripheral vision (walking around vision)  Two consequences  Macular OCT  Laser Treatment
 Mild  The retinal pigment epithelium is  Less invasive  Lasers are not that great, being
 Slow progression damaged and the photoreceptors are  Detects wet AMD abandoned already
 Findings may include subretinal drusen lost (dry AMD)  Optical coherence tomography (OCT)  Anti-VEGF Medications
deposits, focal or more widespread  When it progresses, can damage the acquires cross-sectional images with
geographic atrophy of the retinal pigment Bruch’s membrane and abnormal semihistologic resolution
epithelium (RPE), pigment epithelial vessels can also start growing, which  Monitors progress of wet-AMD
detachments, and subretinal pigment can cause blurring of vision (wet AMD)  It is not practical to repeatedly do
epithelial clumping  May leak and bleed uncontrollably fluorescein angiography
 No real treatment options
Fig 7-25. An area of pigmentary mottling is evident

beneath the retina (arrow). (UpToDate, 2016)
2. Exudative AMD
 Manifestation is primarily a gray membrane,
with exudation
 There is subretinal hemorrhages with
leakage of protein
 Fast progression of loss of central vision
 Treatable to some extent
Fig. 7-26. Top: Normal. Middle: Dry AMD with

patches of atrophy which coalesce to geographic
atrophy – a slow process taking 10 years or so.
Bottom: Wet AMD – new vessels which bleed and
leak eventually leading to scar formation
 Fig. 7-26 Areas of blood vessel leakage are present,
with a large disciform scar (arrow). (UpToDate, 2016)
Hypertensive Retinopathy
 Retinal vascular damage caused by  Acute BP elevation  reversible Table 1. Chronic hypertension grading  Managed primarily by controlling
hypertension vasoconstriction in retinal blood vessels I Increased widened hypertension
 Arteriolar Sclerosis  Hypertensive crisis  optic disk edema reflex/generalized attenuation  Other vision-threatening conditions
 Predisposing factor for veno-occlusive diseases  More prolonged or severe hypertension (generalized narrowing of vessels) should also be aggressively
   endothelial damage and necrosis  Adventitial sheath thickens controlled
 Fundoscopy Findings exudative vascular changes, arteriole wall II AV crossing changes or AV  If vision loss occurs, treatment of the
 AV nicking thickening, arteriovenous nicking nicking retinal edema with laser or with
 In areas where the arteries and veins are  Smoking compounds the adverse effects III Copper wiring intravitreal injection of corticosteroids
crossing in the retina, they share the same of hypertensive retinopathy IV Silver wiring or antivascular endothelial growth
adventitial sheath, so when the vessel factor drug
hardens, the other vessel is impinged   (eg, ranibizumab, pegaptanib, bevaci
 If artery is on top of the vein, it may cause zumab) may be useful
AV nicking
 Cotton wool spots/patches
 Caused by the occlusion of the
precapillary arterioles with ischemic
infarction of the retina
 Flame-shaped hemorrhages
 Depends on which layer you get the
hemorrhage
 In the more superficial layer, the nerve
fiber layer, you can have flame-shaped
hemorrhages
 In the deeper layers, dot-blot Fig. 7-27. Moderate hypertensive retinopathy is
hemorrhages are seen characterized by thinned, straight arteries;
 Optic nerve swelling intraretinal hemorrhages; and yellow hard
 In very severe cases exudates (Prof. J. Wollensak via the Online Journal
 The borders of the nerve are obscured of Ophthalmology)
 Arteriolar sclerotic vascular changes
Table 2. Malignant hypertension grading
 Such a copper or silver wiring (vessels
start to look like copper and then silver 0 No changes
when it is very sclerotic)   I Barely detectable arteriolar
narrowing
 Exudates from exudation of proteins
II Obvious arterial narrowing with
focal irregularities
Box car appearance of the
arteries (mukhang longanisa or
sausage); focal areas of narrowing
III Grade 2 + hemorrhages, cotton
wool spots, retinal edema (present
with exudates)
IV Grade 3 + papilledema
Swelling of the nerve is very
difficult to see in the
ophthalmoscope
Clue is indistinct disc border
 Fig. 7-28. Fundoscopic findings in hypertension
 Fig. 7-29. The cardinal funduscopic feature of

malignant hypertension is optic disk swelling,
which appears as blurring and elevation of disk
margins. The image also shows a characteristic
star-shaped macular lesion caused by leaking
retinal vessels. (Prof. J. Wollensak via the Online
Journal of Ophthalmology)
Central Retinal Vein Occlusion (CRVO)
 Sudden blurring of vision  Patients are usually over 50 years old  Fundoscopy  Manage macular edema
 Two major complications  Associated disease  Extensive retinal hemorrhage  Laser photocoagulation if with
 Reduced vision due to macular edema  Cardiovascular disease  Dilated, tortuous veins neovascularization
 Neovascular glaucoma due to iris  Hypertension  Retinal and macular edema Investigate comorbidities
neovascularization  Hyperlipidemia  Cotton-wool spots representing areas of
 Diabetes mellitus ischemia and infarct
 Collagen-vascular diiseases
 Chronic renal failure
 Hyperviscosity syndromes
 Other risk factors
 Elderly
 Smoking
Figure 7-7. Fundoscopic findings of CRVO, right
eye
 Fluorescein angiography
 Fundus photography
Branch Retinal Vein Occlusion (BRVO)
 Similar to CRVO but affects smaller vein  Same as CRVO  Fundoscopy  Same as CRVO
branches   Small scattered retinal hemorrhages
 Sudden sectoral vision loss  Cotton-wool spots
 Same complications as CRVO  Venous engorgement of affected
vessels
 Figure 7-8. Fundoscopic findings of BRVO, left

eye
Central Retinal Artery Occlusion (CRAO)
 Sudden, painless severe monocular visual  Due to occlusion of central retinal artery  Fundoscopy  Reduce intraocular pressure (IOP)
loss  Results in ischemia and infarction  Attenuated arteries medically
 Occurring over a period of seconds  Causes  Box car appearance  Carbonic anhydrase inhibitor
 VA ranges from counting fngers to light  Thrombus  Visible embolus (possible)  Acetazolamide
perception  Embolus  Cherry red spot at the macula  Dorzolamide
 May be preceded by transient visual loss  Most commonly cholesterol, platelet-  CRaO = Cherry Red spot  Brinzolamide
(amaurosis fugax) fibrin, and calcific  Pale and edematous retina  Beta adrenergic blocker
 Due to a transient ischemic attack  Vasculitis  If perfusion is restored  Timolol
 Episodes of monocular visual loss lasting  Irreversible retinal damage after 90  Fundoscopy appears normal  Dislodge embolus
5-10 minutes minutes of CRAO  But poor vision persists (due to dead  Apply firm, direct pressure on
 “Curtain coming down”  Associated conditions retinal tissue) closed eyes for 15 seconds
 Usually with complete return of vision after  Hypertension  Relative afferent pupillary defect (RAPD) followed by sudden release
the episode  DM  Vasodilation
 Afferent pupillary defect can appear within  Cardiac pathology  Isosorbide Dinitrate (ISDN)
seconds  Carotid atherosclerosis  Nitroglycerine
  Coagulation abnormality (especially if  Increase CO2 levels
young patient)  Paper bag breathing
 Trauma  Carbogen inhalation
 Temporal arteritis (especially in elderly  Anterior chamber paracentesis
patients)  Only if visual loss <24 hours
 Thrombolytics
  Hyperbaric oxygen therapy
 Treat underlying cause
Figure 7-5. Fundoscopic findings of CRAO, right  Investigate for comorbidities
eye Despite all of these, there is still a
 very low chance of success in
recovering vision (poor prognosis)
Branch Retinal Artery Occlusion (BRAO)
 Painless visual field loss  Small embolus is thrown into smaller  Wedge-shaped retinal opacification  Same as CRAO
 Similar to CRAO but has less visual loss unless arterial branches (than in CRAO)
more central branches are affected
Figure 7-6. Fundoscopic findings of BRAO, right

eye

PART C. OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES
CLINICAL MANIFESTATIONS &

PATHOGENESIS DIAGNOSIS TREATMENT
COURSE
CONGENITAL DISEASES
Down Syndrome
 Cataracts
 Early onset: teens to 20’s
 Dislocated lens
 Retinal detachment
 High myopia
 Entropion
 Blepharitis (infection of lid margins)
 Nasolacrimal duct obstruction (due
to facial features)
Marfan Syndrome
 Increased length of long bones,
particularly of fingers and toes
 Ocular manifestations:
 High myopia (due to increase in
growth of the eye)
 Dislocated lens
 Retinal detachment
Phacomatoses
Neurofibromatosis
Type 1: Von Recklinghausen
 Most common phacomatosis  Gene localized to chromosome
 Presents in childhood 17q11
 Café au lait spots
 Pendunculated nodules
 Neurofibromas
 Schwannomas
 Orbital lesions:
 Optic nerve gliomas (unilateral or
bilateral)
 Eyelid neurofibromas
 May cause mechanical
ptosis and external
glaucoma due to the
external pressure on eye
 Intraocular lesions:
 Lisch nodules
Figure 7-33. Lisch Nodules and Choroidal Nevus on NF1
(Image taken from lecture slides of Dr. Valero)
 Not obvious in darkly
pigmented irises
 Very common (95% of
cases)
 Congenital Ectropion Uveae
 Most commonly seen and
visible in Caucasians
 Iris everts and the
pigmentation shows out
 May be associated with
glaucoma
 Choroidal Nevus
 Flat, pigmented lesions
deep in the retina
 Common
 May be multifocal and
bilateral
Type 2: Bilateral Acoustic Neuromas
 Pre-senile cataract (very common)  Defect in chromosome 22
 Combined hamartomas
 RPE/Retina
Figure 7-34. Ocular Lesions of NF2 (Image taken from lecture

slides of Dr. Valero)
Tuberous Sclerosis
 Retinal astrocytoma (“mulberry-
like” tumor)
 Innocuous tumors
 Common: 50%
 May be multiple/bilateral
 Benign state
Figure 7-35. Retinal Astrocytoma (“Mulberry-like tumor)

(Image taken from lecture slides of Dr. Valero)
Von Hippel Lindau Syndrome
 Retinal hemangioma  Angiogram of 
 Very common hemangioma Hemangiomas
 Maybe multiple and bilateral need to be
 Complications: If near the center, cauterized
these vessels can leak (fluid,
exudate, bleeding)
 In late cases  a lot of scarring
and exudations  poor vision
 Multifocal
Figure 7-36. Above: A hemangioblastoma (arrow) in a patient
with von Hippel–Lindau disease, with enlarged retinal arteries
and veins and retinal detachment with hard exudate
(arrowhead). Below: Fluorescein Angiogram. (Image taken
from Ophthalmology: A Pocket Textbook Atlas 2e)
Sturge Weber Syndrome

 Port-wine stain
 Glaucoma
 In the young, it causes
buphthalmos (eyeball becomes
bigger)
 In an older individual, the eyeball
will not get bigger
 Episcleral hemangiomas
 Diffuse choroidal hemangiomas
 Diffuse reddish area
 Sturge-Weber hemangioma vs.
Figure 7-37. Diffuse Choroidal Hemangioma (Image taken VHL hemangioma
from lecture slides of Dr. Valero)  Sturge-Weber: depth is at the
retina
 VHL: depth is at the choroidal
layer
TRAUMATIC DISORDERS
Shaken Baby Syndrome
 Retinal hemorrhages (both pre and  Mother shakes the baby (child  Need to investigate
retinal) abuse)
 Rule out congenital, CT disease and
 Diagnosis of exclusion
as well as a legal matter
leukemia
Figure 7-38. Pre-Retinal and Retinal Hemorrhages in Shaken
Baby Syndrome
VASCULAR DISORDERS
Emboli
Vascular Emboli
 Manifests as acute vision loss  Usually
(similar to branch retinal artery atherosclerotic/cholesterol
occlusion) plaques from carotids
 Talc retinopathy  Can be from heart and heart
 White spots in the retina valves
 History of IV drug abuse
 From inert filter in
methylphenidate hydrochloride
(crystal meth), heroine, and
cocaine
 Talc dissolves in blood and the
Figure 7-40. Figure showing vascular emboli, obstruction mineral may embolize
within the vessel (Image taken from lecture slides of Dr.
Valero)
Amaurosis Fugax
 Sudden painless monocular loss of  Needs careful
vision assessment of
 Transient ischemic attack (ocular cardio/cerebrovascul
version) ar systems
 There is a spasm of vessel
causing loss of vision
 Vision returns to normal within a
few minutes
Figure 7-41. Amaurosis Fugax. (Image taken from

http://www.primehealthchannel.com/amaurosis-fugax.html)
Migraines
 Temporary effects:  Vasospastic phenomenon
 Transient obstruction of vision
 Types:
 Transient visual field loss
 With Headache
 Headaches
 Classic
 Scintillations (scintillating
 If preceded by a migraine aura
scotomas)
 See jagged edges of light that will
 Visual phenomenon or flashing of
lights then followed by a very
last for a few minutes then
severe one-sided throbbing
followed by one-sided throbbing
headache
headaches
 Sometimes with changes in color
 Common
 Periodic headache of varying
without a preceding aura
 Complicated
 Frequent migraine headaches result
in persistent visual or neurological
deficits
 Without Headache
 Ocular/Acephelagic Migraine
 Patient sees light and has ocular
problems after but no headache
Blood Dyscrasias
Hyperviscosity Syndromes
 Usually seen in the young  Causes thrombosis
 Suspect in patients less than 50
years old
 Suspect in patient without
hypertension but presents with
branch/central retinal vein
occlusion
 Blood becomes too thick  vein
occlusion
 Polycythemia
 Multiple myeloma
Figure 7-42. Hemorrhagic Retinopathy on Leukemia (Image  Dysproteinemia
taken from lecture slides of Dr. Valero)
 Leukemia
 Hemorrhagic retinopathy
 Retinal and preretinal hemorrhage
 White centered hemorrhage (Roth
spots) may represent leukemic
infiltration of retina
 APAS (Anti-phospholipid Syndrome)
Thrombocytopenia
 Causes hemorrhage in the retina
Anemia
 Sickle Cell Anemia  Causes ischemia (ischemic
 HbSC disease (most common) retinopathy + neovascularization
 HBSS disease
 Sickle Cell Thalassemia
 Sickling of RBC may produce
retinal arterial occlusions 
neovascularization (sea fan
lesion) at the border of the
perfused and non-perfused retina
 salmon patch lesion when it
bleeds
Figure 7-43. Sickle Cell Anemia. Sickle cell anemia

retinopathy is believed to be vaso-occlusion of peripheral
arterioles of the retina leading to retinal hypoxia, ischemia, and
infarction. New vessels then form at the junction of the vascular
and avascular areas of retina. This neovascularization (Above:
Sea fan lesion) of the retinal tissue and resultant traction of
fibrovascularization places patients at risk for vitreous
hemorrhage (Below: Salmon patch hemorrhage) and retinal
detachment.
NEOPLASTIC DISORDERS
Metastatic Carcinoma
 Most common intraocular  Most common primary site in
malignancy  Females: Breast
 Often see choroidal malignancies  Males: Bronchus (Lungs)
because it is well-perfused
 Maybe asymptomatic in early stages  Other sites:
 Uveitic/Intra-Inflammatory  Kidney, Testis, GI, Prostate
Syndromes are masquerade
syndromes
 Looks like uveitis but might be
malignancy
Figure 7-44. Metastatic Carcinoma (Image taken from lecture  If patient does not respond to
slides of Dr. Valero) therapy, work-up for this
 Redness
 Blurring
AUTOIMMUNE DISORDERS
Connective Tissue DIsease
 Dry eyes/Keratoconjunctivitis
sicca
 Burning sensation
 Foreign body sensation
 Photophobia
Sjögren’s Syndrome
 Dryness of all mucus membranes  Anti-SS-A/Anti-RO
 Dry mouth
 Dry eyes
 No glossy appearance of cornea
Figure 7-45. Sjogren’s Syndrome ocular manifestations (Image

taken from lecture slides of Dr. Valero)
Ankylosing Spondylitis
 Usual in young males between 20-  Chronic inflammatory arthritis of
40 years old unknown etiology
 Incidence of uveitis in AS: 30%
 Predominantly affects the axial
 30% of males with uveitis will skeleton (spine and sacrum) not limbal
develop AS skeleton
 History:  Early diagnosis can prevent development
 Blurring of vision of severe structural changes in the spine
 Recurrent history of lower back
pains
 Young males with uveitis should
Figure 7-46. Ankylosing Spondylitis (Image taken from lecture have an X-ray of sacroiliac joints
slides of Dr. Valero)  25% with AS will have one or more
attacks of iritis
 Precede clinical arthritis
 Photophobia, redness, decreased
vision
 Acute recurrent non-
granulomatous iridocyclitis
(uveitis)
 Invariably unilateral
Rheumatoid Arthritis
 Dry Eyes
 Episcleritis
 Just superficial
 Usually not painful
 Put phenylephrine and it will
blanch more superficial vessels,
which is the episcleritis and not
scleritis
 Scleritis
 Deeper layers are involved
 Tender
 Necrosis
 Peripheral corneal ulceration
Figure 7-47. Rheumatoid Arthritis (Image taken from lecture
slides of Dr. Valero)
Systemic Lupus Erythematosus

 Dry Eyes
 Scleritis
 Peripheral corneal ulcers
 Retinopathy
 Optic Neuropathy
 Most common: vasculitis, phlebitis
 Lots of exudate and cotton wool
spots
Figure 7-48. Systemic Lupus Erythematosus (Image taken

from lecture slides of Dr. Valero)
Giant Cell/Temporal Arteritis
 Diseases of elderly patients (mostly  To diagnose, you will
women over age 60) have to take a biopsy
 Jaw claudication of the artery
 Headache
 Scalp tenderness
 Especially in the area of the
temporal artery
 Fever
 Weight loss
 Fatigue
 Myalgias
 Acute visual loss
 Cranial nerve palsy
 Ischemic optic neuropathy
 Due to central artery occlusion
 Temporal arteritis
Figure 7-49. Giant Cell Tempral Arteritis gross inspection and
fundus examination (Image taken from lecture slides of Dr.
Valero)
Thyroid Eye Disease

 Ocular signs and symptoms  Thyroid-associated
precede, follow, or coincide with ophthalmopathy/Graves’ Disease
hyperthyroidism
 10-25% are euthyroid (Euthyroid
 Systemic Autoimmune Disorder
Graves’ Disease)  Thyroid gland (Hyperthyriodism)
 Soft tissue involvement  Orbit (Infiltrative Orbitopathy)
 Restrictive myopathy  Infiltrative Dermopathy (Pretibial
Myxedema)
Figure 7-50. Thyroid eye disease manifestation – Proptosis
 Optic neuropathy
(Image taken from lecture slides of Dr. Valero)  Eyelid retraction
 Upper and lower lid retraction
exaggerates orbital protrusion due
to infiltration of extraocular
muscles
 Proptosis
 Failure to blink can cause a
corneal ulcer
 Corneal involvement
 Corneal Ulceration
 Most common cause of
blindness in thyroid
ophthalmology
 EOM swelling
Multiple Sclerosis
 Ataxia, dysarthria, extremity  Autoimmune disorder with focal
weakness, hemiparesis, depression, patchy destruction of white matter in
fatigue, frequency, urgency, the brain, spinal cord and optic
incontinence, diplopia, blurred nerves
vision
 Optic Neuritis is the presenting
 Demyelination occurs
sign in 25% of MS cases
 1/3 papillitis (swollen nerve,
obscured borders), 2/3 retrobulbar
(nerve will appear normal at first
then it becomes pale if chronic)
Figure 7-51. Multiple Sclerosis  74% F, 34% M will develop MS
within 15 years of initial attack of
optic neuritis
 Color perception never goes back
 Color saturation is bad
 If you see optic neuritis, with
decreased saturation in color and
relative afferent pupillary defect, it
is most probably MS
Myasthenia Gravis
 ½ will present with ocular signs, the  Disorder of the neuromuscular
rest will develop ocular symptoms junction
during the course  All muscles can be affected, including
 Ptosis is usually the complaint those of the eyes and the eye lids
 Alternating ptosis is MG until  Systemic or ocular muscles affected
proven otherwise
 Gets worse as the day
progresses (afternoon)
Figure 7-52. Patient with Myasthenia Gravis – Ptosis worse in
the afternoon (Image taken from lecture slides of Dr. Valero)
Behcet’s Disease
 Clinical triad of:  Idiopathic multisystem disease:
 Recurrent oral ulcerations Obliterative vasculitis
 Genital ulceration
 Most common ocular
presenting sign: Uveitis
 70% develop bilateral non-
granulomatous intraocular
inflammation, either anterior or
posterior uveitis
Figure 7-53. Behcet’s disease (Image taken from lecture slides  Other manifestations:
of Dr. Valero)  Skin lesions: pustules, erythema
nodosum, ulceration
Vogt-Kotanagi-Harada Syndrome
 Skin:
 Poliosis (whitening of eyelashes)
 Vitiligo (patches of skin
depigmentation)
 Alopecia (baldness)
 CNS/Neurologic:
 Encephalopathy
 CSF lymphocytosis
 Auditory Symptoms:
 Tinnitus
 Vertigo
Figure 7-54. Fundoscopic findings of Vogt-Koyanagi-Harada
disease (Image taken from lecture slides of Dr. Valero)
 Deafness
 Uveitis: Anterior and Posterior
 Exudative Retinal Detachment
 This can mimic an intraocular
malignancy
INFECTIOUS
Acquired Systemic Syphilis
 Madarosis (loss of  A venereal chronic infection caused  Ocular involvement  Tertiary
eyebrows/eyelashes) by a spirochete called Treponema is strongly suggestive syphilis will
 Iridocyclitis pallidum of tertiary syphilis, so require IV
 Precipitates underneath cornea  Stages: do work-up for CNS antibiotic
 Periphlebitis  Primary involvement therapy
 Pale vessels with hemorrhage  Painless indurated genital
around chancre at the site of
 Neuroretinitis (optic atrophy) inoculation and regional
adenopathy
 Commonly presents during
secondary/tertiary syphilis  Secondary
 Ensues 6-8 weeks after the
Figure 7-55. Syphilis ocular manifestations (Image taken chancre
from http://www.newhealthguide.org/Pdr.html)
 Maculopapular skin lesions
(palms and soles)
 Latent
 Follows resolution of
secondary syphilis and can
be detected only by
serological tests
 Tertiary
 15-25% will progress to this
stage associated with
neurosyphilis,
cardiovascular syphilis, and
gummata (nodular indolent
granulomas)
Tuberculosis
 Most common finding is  Intractable uveitis unresponsive
granulomatous iridocyclitis to steroid therapy
 Mutton fat keratic precipitates  Virtually any ocular and periocular
sticking at back of endothelium structure can be involved
 Choroidal granuloma
Figure 7-56. Ocular tuberculosis manifestations (Image

taken from http://www.newhealthguide.org/Pdr.html)
HIV/AIDS
 Ocular involvement may be the
presenting symptom of HIV/AIDS
 Dry eyes
 HIV retinopathy
 Mimics HPN and DM
retinopathy
 If a young patient with no
comorbidities presents with this
kind of retinopathy, try to elicit
sexual history and other high-
risk behavior
 Cotton wool patches
Figure 7-57. Kaposi’s sarcoma on eyelid of HIV/AIDS  If CWP only, think HIV AIDS
patient (Image taken from  CMV retinitis
http://www.newhealthguide.org/Pdr.html)  Kaposi’s sarcoma eyelids (not
common now)
Toxoplasmosis
 Primary lesion is retinitis and  Infestation by an obligatory
granulomas intracellular protozoan parasite:
Toxoplasma gondii
 Definitive hosts: cats
 Intermediate hosts: humans (mice
and livestock)
 Infected via:
 Ingestion of undercooked meat
 Direct ingestions of oocytes
 Transplacental
 Stages:
Figure 7-58. Toxoplasmosis (Image taken from  Acute
http://www.newhealthguide.org/Pdr.html)  Ingestion, parasites penetrate
intestinal mucosa, blood
stream, disseminated
throughout the body
 Enters RES cells, brain,
retina, lungs, striated muscles
 Chronic inactive
 Intracellular cyst formation
 Recurrent
 Reactivated when immune
system is down
Toxocariasis
 Chronic Endophthalmitis  Infection caused by a common
 Vitreous abscess intestinal roundworm of cats
 Peripheral granuloma (Toxocara cati) and dogs
(Toxocara canis)
 Posterior pole granuloma
 Infection due to ingestion of soil or
food contaminated with dog feces
(with ova)
 Ova develop into larvae, penetrate
intestinal wall, and travel to various
organs (liver, lungs, skin, brain, and
eyes)
Figure 7-59. Toxocariasis (Source:

http://www.newhealthguide.org/Pdr.html)
Herpes Zoster Ophthalmicus
 Painful crusty, vesicular lesions  Follows distribution of CN V1
along distribution of nerve
 Corneal stromal keratitis
 Intraocular involvement
 Uveitis
 40% likely if the tip of the nose is involved
(Hutchinson’s sign)
 Retinitis
 Neuritis  Prevalence increases with age due
to reactivation potential
 In patients under 40 years old,
suspect HIV
Figure 7-60 Patient with Herpes Zoster Ophthalmicus.

Note how the lesions follow the distribution of CN V1 and
presence of Hutchinson’s sign (involvement of the nasal
tip) (Image taken from http://reference.medscape.com)
DRUGS/TOXINS
 Systemic medications with significant
ocular effects:
 Toxic retinopathy (presents as
macular deposits)
 Thioridazine
 Chloroquine (would usually
show as a bull’s eye
retinopathy)
 Hydroxychloroquine (would
usually show as a bull’s eye
retinopathy)
 Tamoxifen
 Used for treatment of breast
cancer
 Important to do a periodic
eye examination
 Tamoxifen toxic retinopathy
is reversible if you stop or
decrease the dosage
 Toxic Optic Neuropathy
 Ethambutol (irreversible)
 Most significant in the
Philippines
 Visual loss is irreversible
 Important to do baseline eye
tests and periodic screening
thereafter
 Isoniazid

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07 OPHTHALMOLOGY

PART A. Basic Eye Exam- VAGETF

VISUAL ACUITY GROSS EXAM EXTRAOCULAR MUSCLES TONOMETRY FUNDOSCOPY

PART B. Common Eye Diseases

CLINICAL MANIFESTATIONS & COURSE PATHOGENESIS DIAGNOSIS TREATMENT

6. Completion- aspiration of remaining

 Other surgical methods of

 Overview of Age-related Cataract  Cataract Maturity

 Complications of Age-related Cataract

Fig.7-8. Nuclear cataract

Fig.7-9 Immature vs mature cataract

3. Hypermature lens- shrunken and wrinkled

Acute angle-closure glaucoma

Fig.7-13 Normal anterior chamber angle via

Fig.7-17. Post-laser iridotomy

Fig.7-14. AAG with ciliary injection, mid-dilated

Acute Anterior Uveitis (AAU)

Fig.7-19. AA Uveitis, gross

Fig.7-20. Cells and Flare

Diabetic Retinopathy (DR)

Fig. 7-20 Color fundus photograph of nonproliferative

2. Proliferative Diabetic Retinopathy

Fig 7-21 Color fundus photograph of proliferative diabetic

3. Diabetic Macular Edema (ME)

Fig 7-24. (A) Optical coherence tomography (OCT) of

Fig 7-25. An area of pigmentary mottling is evident

Fig. 7-26. Top: Normal. Middle: Dry AMD with

 Fig. 7-29. The cardinal funduscopic feature of

 Figure 7-8. Fundoscopic findings of BRVO, left

Figure 7-6. Fundoscopic findings of BRAO, right

PART C. OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES

CLINICAL MANIFESTATIONS &

Figure 7-34. Ocular Lesions of NF2 (Image taken from lecture

Figure 7-35. Retinal Astrocytoma (“Mulberry-like tumor)

Sturge Weber Syndrome

Figure 7-41. Amaurosis Fugax. (Image taken from

Figure 7-43. Sickle Cell Anemia. Sickle cell anemia

Figure 7-45. Sjogren’s Syndrome ocular manifestations (Image

Systemic Lupus Erythematosus

Figure 7-48. Systemic Lupus Erythematosus (Image taken

Thyroid Eye Disease

Figure 7-56. Ocular tuberculosis manifestations (Image

Figure 7-59. Toxocariasis (Source:

Figure 7-60 Patient with Herpes Zoster Ophthalmicus.

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