4. Eye examinationEye examination
VisionVision
External – Look at eyelids, make sure everything looks normal.External – Look at eyelids, make sure everything looks normal.
PupilsPupils
Relative afferent papillary defectRelative afferent papillary defect
See if pupils are reacting normallySee if pupils are reacting normally
Motility – Have the patient look up, down, right and left.Motility – Have the patient look up, down, right and left.
Exam of anterior segmentExam of anterior segment
Dilated ophthalmoscopy – Examine retina, optic nerve, andDilated ophthalmoscopy – Examine retina, optic nerve, and
vessels.vessels.
Visual fields – Place you finger in different places in patientVisual fields – Place you finger in different places in patient’’ss
visual field and ask him if he sees it. Test one eye at a time.visual field and ask him if he sees it. Test one eye at a time.
9. VascularVascular disorders with oculardisorders with ocular
manifestationsmanifestations
HypertensionHypertension
MigrainesMigraines
EmboliEmboli
Amaurosis fugaxAmaurosis fugax
10. Vascular HypertensionVascular Hypertension
Affects eyes the same way it affects the rest ofAffects eyes the same way it affects the rest of
the bodythe body
–– Arteriolar sclerosisArteriolar sclerosis
–– Direct pressure damageDirect pressure damage
Number one predisposing factor for otherNumber one predisposing factor for other
eye disorders like CRVO, BRVOeye disorders like CRVO, BRVO
11. Vascular HypertensionVascular Hypertension
In a normal eye, the vessel walls areIn a normal eye, the vessel walls are
transparent - you see the blood (red)transparent - you see the blood (red)
Arteriolar sclerosis causing thickening of theArteriolar sclerosis causing thickening of the
vessel wallsvessel walls
–– Early sclerosis -Early sclerosis - ““copper wirecopper wire”” vesselvessel
appearanceappearance
–– More sclerosis -More sclerosis - ““silver wiresilver wire”” appearanceappearance
12. Vascular HypertensionVascular Hypertension
Arteries and veins share the same sheathArteries and veins share the same sheath
As arteriolar walls sclerose and thicken, the veinAs arteriolar walls sclerose and thicken, the vein
is compressed - AV Nickingis compressed - AV Nicking
13. Vascular HypertensionVascular Hypertension
Acutely elevated blood pressure can lead toAcutely elevated blood pressure can lead to
fibrinoid necrosis of blood vessel wallsfibrinoid necrosis of blood vessel walls
–– Get exudates, cotton wool spots,Get exudates, cotton wool spots,
hemorrhageshemorrhages
–– Can also see macular edema, nerveCan also see macular edema, nerve edemaedema
17. Vascular HypertensionVascular Hypertension
Classically, it is taught that hypertensivesClassically, it is taught that hypertensives
should be referred for ophthalmologicshould be referred for ophthalmologic
evaluationevaluation
–– No point in this - we canNo point in this - we can’’t do anythingt do anything
–– Send them to their primary care physician forSend them to their primary care physician for
BP controlBP control
–– To the emergency room if systolic BP overTo the emergency room if systolic BP over
200.200.
18. Vascular MigrainesVascular Migraines
Migraines are a vasospastic phenomenonMigraines are a vasospastic phenomenon
Usually the effects are temporary, but theyUsually the effects are temporary, but they
can be permanent - like a strokecan be permanent - like a stroke
19. Vascular MigrainesVascular Migraines
Ocular manifestationsOcular manifestations
–– ScintillationsScintillations
–– Transient homonymous hemifield lossTransient homonymous hemifield loss
–– Transient cortical visual lossTransient cortical visual loss
–– Amaurosis fugaxAmaurosis fugax
–– Rarely, CRAO or BRAORarely, CRAO or BRAO
20. Vascular MigrainesVascular Migraines
TreatmentTreatment
–– Prevent frequent attacksPrevent frequent attacks
–– Examine for visual lossExamine for visual loss
–– Consider discontinuation of oralConsider discontinuation of oral
contraceptives as they can lead to thromboticcontraceptives as they can lead to thrombotic
eventsevents
21. Vascular EmboliVascular Emboli
Usually are atherosclerotic/cholesterolUsually are atherosclerotic/cholesterol
plaques from the carotidsplaques from the carotids
Can be from other sourcesCan be from other sources
–– heart and heart valvesheart and heart valves
–– IV drug abuse - talcIV drug abuse - talc
Manifests as acute visual loss such asManifests as acute visual loss such as
CRAO, BRAOCRAO, BRAO
25. Vascular Amaurosis fugaxVascular Amaurosis fugax
Sudden, painless monocular loss of visionSudden, painless monocular loss of vision
–– Usually manifests likeUsually manifests like ““a window shadea window shade
coming downcoming down”” or dimmingor dimming
–– By definition, vision returns to normal withinBy definition, vision returns to normal within
a few minutesa few minutes
Caused by temporary arterial occlusionCaused by temporary arterial occlusion
33. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
Most common cause of blindness in theMost common cause of blindness in the
U.S. between the ages of 18 and 74U.S. between the ages of 18 and 74
8000 people become blind annually in U.S.8000 people become blind annually in U.S.
Many effects on the eyeMany effects on the eye
- Changes refraction- Changes refraction
- Causes cataracts- Causes cataracts
- Most important is retinopathy- Most important is retinopathy
34. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
Ocular problems are a function of durationOcular problems are a function of duration
of diseaseof disease
- 5 years - 23%- 5 years - 23%
- 20 years - 90%- 20 years - 90%
- 30 years - 99%- 30 years - 99%
- Rare in children under 10 regardless of- Rare in children under 10 regardless of
duration of diseaseduration of disease
35. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
Nonproliferative diabetic retinopathy (NPDR)Nonproliferative diabetic retinopathy (NPDR)
–– Capillaries develop leaks and occludeCapillaries develop leaks and occlude
–– See microaneurysms, dot/blot hemorrhages,See microaneurysms, dot/blot hemorrhages,
exudates, and macular edemaexudates, and macular edema
–– Vision loss at this stage is from macular edemaVision loss at this stage is from macular edema
39. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
NPDRNPDR
–– As it becomes more severeAs it becomes more severe
•• Marked vascular tortuosityMarked vascular tortuosity
•• More hemorrhagesMore hemorrhages
•• Cotton wool spotsCotton wool spots
40. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
Proliferative diabetic retinopathy (PDR)Proliferative diabetic retinopathy (PDR)
–– Due to ischemiaDue to ischemia
–– Neovascularization - usually on nerve headNeovascularization - usually on nerve head
–– Vessels bleed into vitreousVessels bleed into vitreous
–– Fibrous tissue develops and causes tractionalFibrous tissue develops and causes tractional
retinal detachmentsretinal detachments
–– PROFOUND visual lossPROFOUND visual loss
45. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
PDRPDR
–– Needs prompt treatment to preventNeeds prompt treatment to prevent vitreousvitreous
hemorrhages and retinalhemorrhages and retinal detachmentsdetachments
–– Treatment causes regression of theTreatment causes regression of the vesselsvessels
–– Treatment reduces visual loss by 50%Treatment reduces visual loss by 50%
46. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
PDRPDR
–– TreatmentTreatment
•• Scatter 1000-3000 laser burnsScatter 1000-3000 laser burns
throughout retinathroughout retina
•• Avoid maculaAvoid macula
•• Decreases retinal oxygen need whichDecreases retinal oxygen need which
decreases the impetus fordecreases the impetus for
neovascularizationneovascularization
•• Treatment needs to be ongoingTreatment needs to be ongoing
48. EndocrineEndocrine
Diabetes MellitusDiabetes Mellitus
The only thing that has been shown to delay theThe only thing that has been shown to delay the
onset of and/or decrease the severity of diabeticonset of and/or decrease the severity of diabetic
eye disease is controlling the blood sugar - up toeye disease is controlling the blood sugar - up to
76% reduction!76% reduction!
All diabetics need an eye exam at least once perAll diabetics need an eye exam at least once per
yearyear
50. AutoimmuneAutoimmune
Connective Tissue DiseasesConnective Tissue Diseases
Dry eyes are the most common manifestationDry eyes are the most common manifestation
Symptoms:Symptoms:
–– BurningBurning
–– PhotophobiaPhotophobia
–– Foreign body sensationForeign body sensation
54. AutoimmuneAutoimmune
GravesGraves’’ diseasedisease
Improperly calledImproperly called ““thyroid eye diseasethyroid eye disease””
Immune system attacks both thyroid glandImmune system attacks both thyroid gland
and extraocular muscles (EOM)and extraocular muscles (EOM)
Not related to thyroid hormone levelsNot related to thyroid hormone levels
Can progress even when euthyroidCan progress even when euthyroid
60. AutoimmuneAutoimmune
GravesGraves’’ diseasedisease
Treatment - as neededTreatment - as needed
–– Artificial tearsArtificial tears
–– Oral steroidsOral steroids
–– Strabismus surgeryStrabismus surgery
–– Lid surgeryLid surgery
–– Orbital decompression surgeryOrbital decompression surgery
–– Orbital radiationOrbital radiation
61. AutoimmuneAutoimmune
Myasthenia gravisMyasthenia gravis
Autoimmune reaction to the acetylcholineAutoimmune reaction to the acetylcholine
receptors in muscle tissuereceptors in muscle tissue
Ocular manifestations:Ocular manifestations:
–– PtosisPtosis
–– StrabismusStrabismus
–– Facial weaknessFacial weakness
–– Worse at the end of the day - fatiguesWorse at the end of the day - fatigues
easilyeasily
63. AutoimmuneAutoimmune
Myasthenia gravisMyasthenia gravis
Other manifestations:Other manifestations:
–– Proximal limb weaknessProximal limb weakness
–– Difficulty swallowing or breathing (which canDifficulty swallowing or breathing (which can
be deadly)be deadly)
–– Sometimes triggered by an underlyingSometimes triggered by an underlying
thymoma - always get chest CTthymoma - always get chest CT
64. AutoimmuneAutoimmune
Myasthenia gravisMyasthenia gravis
Confirm diagnosis with edrophonium (Tensilon)Confirm diagnosis with edrophonium (Tensilon)
test and checking for acetylcholine receptortest and checking for acetylcholine receptor
antibodiesantibodies
Treatment:Treatment:
–– Oral anticholinesterase (e.g. pyridostigmine)Oral anticholinesterase (e.g. pyridostigmine)
–– SteroidsSteroids
–– Immunosuppressive therapyImmunosuppressive therapy
–– Surgical removal of any thymomaSurgical removal of any thymoma
74. Idiopathic SarcoidosisIdiopathic Sarcoidosis
Generalized, multisystem inflammatoryGeneralized, multisystem inflammatory
disorderdisorder
25% exhibit ocular manifestations25% exhibit ocular manifestations
Much more common in blacks andMuch more common in blacks and
hispanics than whiteshispanics than whites
82. Infectious HIV/AIDSInfectious HIV/AIDS
CMV retinitisCMV retinitis
–– Leading cause of visual loss in AIDSLeading cause of visual loss in AIDS
–– 25% of AIDS patients get it25% of AIDS patients get it
–– CD4 <50CD4 <50
–– Hemorrhagic necrosis of retinaHemorrhagic necrosis of retina
–– Indicates poor prognosis for survivalIndicates poor prognosis for survival
–– Fortunately, infrequently seen since advent ofFortunately, infrequently seen since advent of
protease inhibitorsprotease inhibitors
84. Infectious HIV/AIDSInfectious HIV/AIDS
Treatment of CMV retinitis:Treatment of CMV retinitis:
–– IV ganciclovirIV ganciclovir
–– IV foscarnetIV foscarnet
–– Intravitreal ganciclovirIntravitreal ganciclovir
–– Ganciclovir sustained-release intravitrealGanciclovir sustained-release intravitreal
implantsimplants
85. Infectious Herpes ZosterInfectious Herpes Zoster
OphthalmicusOphthalmicus
10-15% of zoster is ocular10-15% of zoster is ocular
Follows distribution of V1Follows distribution of V1
Eye is often involvedEye is often involved
- Roughly 5-10%- Roughly 5-10%
- Roughly 40% if tip of nose involved- Roughly 40% if tip of nose involved
86. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
Prevalence increases with agePrevalence increases with age
In patients under 40 - suspect HIVIn patients under 40 - suspect HIV
90. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
Treatment:Treatment:
–– Oral acyclovir 800mg 5x/day (or IV)Oral acyclovir 800mg 5x/day (or IV)
–– Should be started within 7 days of onsetShould be started within 7 days of onset
–– With eye involvement:With eye involvement:
•• Topical steroids (not trifluridine)Topical steroids (not trifluridine)
•• LubricationLubrication
Notas do Editor
Will see hamartomas (Lisch nodules).
95% of neurofibromatosis I pts present with hamartomas by age 6.
Intracranial Hypertension: Causes
(Brain swelling causes pressure down the dural sheath to the optic nerve,
leading to swelling of the optic nerve head.)
Causes:
- Brain Tumor
- Meningitis
- Venous sinus thrombosis
- Hydrocephalus
- Idiopathic intracranial HTN – A diagnosis of exclusion. (most common)
Central Retinal Artery Occlusion:
- Internal carotid artery ophthalmic artery central retinal artery
- Anything clogging the vasculature along this line will cause ischemia of the eye.
Causes:
- Occlusion of ophthalmic artery – total ocular ischemia
- Central retinal artery – ischemia of the retina
- Either way there is vision loss that is typically painless
Management: Goals are to lower pressure in the eye and vasodilate the vessels in the eye.
The following treatments will do this.
- Rebreathing CO2 – Have patient breathe in a plastic bag to dilate the vessels.
- Topical β-blockers – Lower the pressure
- IV acetazolamide 500 mg
- Massaging of globe with lids closed: Massage with heel of your hand to dislodge the plaque
that is causing the occlusion.
- Anterior chamber paracentesis
- Calcium channel blockers
- Hyperbaric O2
Hypertension: Factors Affecting Retinal Arterioles
- Severity
- Duration:
- Acute – Severe hemorrhaging, exudates
- Chronic – Narrowing of arterioles, copper-wiring (looks like silver streak overlying the arteriole), some hemorrhaging but not as severe as in acute because the vessels have thickened over the years.
Types:
- With headache – Classic, common, complicated
- Without headache - Acephalgic – All the symptoms of a classic migraine, except no headache
Visual Symptoms:
- Scintillations – Aura - Usually bilateral. Sometimes a pt will report that it’s only in their right eye, but if they close their right eye they can still see the scintillations. They actually mean the aura is in their right visual field. Usually lasts 10-45 minutes.
- Amaurosis fugax – Sudden painless visual loss. Seen in very severe migraines.
- Transient homonymous hemifield loss
- Transient cortical blindness – Seen in very severe migraines
Amaurosis Fugax
- Term for symptoms caused by embolic phenomenon.
- Monocular dimming of vision
- Temporary arterial obstruction – As plaque moves along the vasculature, areas that were ischemic get reperfused, so areas of decreased vision go away.
- Sudden, transient, painless visual loss
Evaluation:
- Cardiovascular – Look at heart for source of embolization (pts with mitral valve prolapse have plaques on their valves that can break off)
- Cerebrovascular – Usually look at carotid arteries
- Ophthalmologic – Sometimes you can see the plaque, which will lead to the diagnosis.
Ocular symptoms of Hyperviscosity Syndromes:
- Amaurosis fugax
- Permanent visual loss
Malignant Neoplasms Involving the Eye
- Primary ocular melanoma – Most common primary tumor of the eye.
- Large cell lymphoma
- Metastatic carcinoma – Most common tumor of the eye.
Metastatic Carcinoma
- Most common intraocular malignancy in adults
- May be asymptomatic
- May produce decreased or distorted vision
- Less common in the iris because less vasculature in iris than in choroid
- Multiple tumors or bilateral involvement mean metastatic carcinoma.
Ocular Metastasis:
Treatment
- Local radiation
- Chemotherapy
- Eye wall resection
- Enucleation if blind, painful eye
- Ophthalmologist should monitor ocular metastases at regular intervals
- You can observe ocular metastases to see if treatment of the 1° tumor is working.
(Meaning if the tumor in the eye is growing, then the treatment is not working.)
Sickle Cell Retinopathy
- HbSC disease (most common form) – Most common form to cause the peripheral neovascularization seen in sickle cell retinopathy. Causes neovascularization out in the periphery of the fundus.
- Mechanism of neovascularization – Occluded arteries in the periphery of the fundus retina becomes ischemic retina sends out factors in response to ischemia new blood vessels made, but the new vessels leak and bleed easily.
- Treatment – Ablate the retina with laser so it produces fewer factors.
- HbSS disease
- Sickle thalassemia
Sjogren’s Syndrome
- Dry eyes
- Dry mouth
- May have connective tissue disorder
- You can look for specific autoantibodies if you suspect Sjogren’s syndrome
Ankylosing Spondylitis: Ocular Symptoms
- Photophobia
- Redness
- Decreased vision
- Iritis – Inflammation inside the eye. Can see WBC’s floating around inside the eye.
Polyarteritis Nodosa: Ocular Manifestations
- Dry eyes
- Corneal ulcers
- Scleritis
- Hypertensive retinopathy
- Retinal vasculitis
Giant Cell Arteritis
Ischemic optic neuropathy caused by GCA
- Mechanism:
Thickening of the arteries lumen becomes smaller and smaller artery can eventually close
ischemia of the optic nerve head, which is typically irreversible and untreatable.
- The only thing that we can do then is treat the temporal arteritis,
and try to prevent the same thing from happening in the other eye.
- Usually leads to legal blindness in the affected eye
(may not be totally blind, but the eye is basically useless).
- If GCA goes untreated, pt can permanently lose vision in opposite eye
within hours to days, so treat aggressively.
- Symptoms:
- Headache
- Scalp tenderness
- Jaw claudication
- Polymyalgia rheumatica
- Tenderness to palpation of temporal artery area
- Acute visual loss – Typically in older pt (above 60)
- Diagnosis:
- Clinical history
- STAT ESR – If ESR is high and you’re very suspicious for GCA,
go ahead and treat. BUT, ESR is negative in 20% of cases of GCA, so history is key.
- Fluorescein angiogram
- Temporal artery biopsy – Start treatment before you biopsy.
- Treatment:
- If GCA is suspected, begin treatment immediately with high-dose corticosteroids daily.
- A temporal artery biopsy can be done
within a week after treatment with high-dose steroids has begun and still show positive results.
- Do not wait for results of temporal artery biopsy to begin treatment.
- Treatment will not produce immediate changes in the artery,
but it will prevent the same thing from happening in the other eye.
- Once the diagnosis is confirmed with the biopsy,
follow the patient with ESRs. If ESR becomes elevated, repeat treatment with steroids.
Topical corticosteroids may lead to serious ocular complications – As a Primary Care Physician,
never treat pts with topical steroids. Unless you have a slit lamp and you can really see the cornea and conjunctiva under high magnification, you’re going to miss some things and possibly mistreat a pt’s condition with topical steroids. Treatment with topical steroids for a prolonged period of time can lead to glaucoma, cataracts, and infections.
Dry Eyes: Treatment
- Artificial tears
- Lubricating ointment at night
- Punctal occlusion
- Environmental modification – As in goggles, humidifier in the bedroom, don’t leave ceiling fan on.
- Severe dry eyes epithelium of the eye sloughs off stroma underneath “melts” perforation of the globe and the iris is “mashed” up against the cornea (loss of the space in between the two structures)
Cotton-wool spots – Micro-infarction from occluded vasculature
Thyroid Ophthalmopathy: Classes – acronym - NOSPECS
0 – No signs or symptoms
1 – Only signs – Such as lid retraction. Tell the patient to look up then look down;
a sign of thyroid eye disease is if the eyelid lags behind when the pt looks down.
2 – Soft tissue involvement – May have dry eye type symptoms
3 – Proptosis – Thyroid/Graves’ disease is most common cause of uni- or bilateral proptosis.
If you find undiagnosed proptosis, look at thyroid function.
4 – Extraocular muscle involvement – Restriction of eye motility.
Inferior rectus is the most common muscle affected.
5 – Corneal damage – Due to exposure because the patient can’t close their eye.
Can be prevented by maximal lubrication and other treatments.
6 – Sight loss
Mechanism of compressive optic neuropathy:
Lymphocytic infiltrates in extraocular muscles muscles get so big they take up
all the space in the orbit muscles compress the optic nerve sight loss
Thyroid Ophthalmopathy:
Treatment of Congestive Phase (usually within first 2 years of onset of symptoms):
- Tear substitutes
- Systemic corticosteroids – To decrease inflammation in the orbit.
- Orbital irradiation or surgical decompression
Surgical decompression – Knock out the floor of the orbit to allow
some of the orbital contents to go into the maxillary sinus so that
the nerve is not compressed.
Treatment of Cicatricial Phase (damage is done; disease not progressing anymore):
- Lid surgery – To lower the lid so it covers the eye better.
- Muscle surgery
- Orbital surgery
Myasthenia Gravis: Systemic Involvement
Typical history – In the morning, the patient is ok.
Towards the end of the day, the patient can’t keep his eyes open, has double vision.
Refer suspected patients for neurologic evaluation
Rheumatoid Arthritis: Ocular Manifestations
- Dry eyes
- Episcleritis – Inflammation of the superficial sclera.
- Scleritis – Inflammation of the sclera
- Corneal ulcers
- Uveitis
Scleromalacia perforans – A slow, quiet inflammation; pt probably won’t know it’s there.
“Melts” the sclera. You can see it if you lift the pt’s eyelid and have them look down.
Tell the pt not to rub eyes because the sclera is so thin that minimal trauma can perforate it.
Pauci-articular – Most common form affecting the eye.
So if there are only 2 or 3 joints involved, then the patient is more likely to have ocular manifestations
than a patient with every joint involved
Iritis in Juvenile Rheumatoid Arthritis:
- Few symptoms or signs
- Usually chronic
- Secondary cataract and glaucoma
- Periodic ophthalmic screening; because findings are very subtle,
and if untreated, it could lead to glaucoma, cataracts, and scarring inside the eye.
Optic Neuritis
- May be initial manifestation of MS
- Acute, painful (unlike amaurosis fugax, which is painless) vision loss in one or both eyes0
- May have afferent papillary defect
- Treat initial episode with IV methylprednisolone
- Idiopathic inflammation
Causes a specific form of iritis:
can see WBC floating around in the eye (“mutton fat”), severe photophobia.
Refer patients with sarcoidosis if ocular involvement is suspected.
Treatment may include corticosteroids.
AIDS: Ocular Manifestations
- Dry eye
- Cotton-wool spots – Whitish spots due to occlusion of a vessel.
- CMV retinitis
- Kaposi’s sarcoma involving the eyelid or conjunctiva