Ocular manifestations of systemic disease
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Ocular manifestations of systemic disease
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Ocular manifestations of systemic disease
- 1. Ocular ManifestationsOcular Manifestations of Systemic Diseaseof Systemic Disease Dr. Riyad G. BanayotDr. Riyad G. Banayot
- 3. Categories of systemic diseaseCategories of systemic disease CongenitalCongenital VascularVascular Endocrine/MetabolicEndocrine/Metabolic AutoimmuneAutoimmune IdiopathicIdiopathic InfectiousInfectious Drugs/ToxinsDrugs/Toxins NeoplasticNeoplastic TraumaTrauma
- 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.
- 5. CongenitalCongenital disorders with oculardisorders with ocular manifestationsmanifestations Down SyndromeDown Syndrome Marfan's SyndromeMarfan's Syndrome Myotonic DystrophyMyotonic Dystrophy Tuberous SclerosisTuberous Sclerosis Congenital Metabolic DisordersCongenital Metabolic Disorders Lysosomal storageLysosomal storage Carbohydrate metabolismCarbohydrate metabolism NeurofibromatosisNeurofibromatosis
- 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
- 22. Emboli affecting the eyesEmboli affecting the eyes
- 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
- 26. Vascular Blood DyscrasiasVascular Blood Dyscrasias Hyperviscosity syndromes - thrombosisHyperviscosity syndromes - thrombosis –– Including polycythemia, myeloma,Including polycythemia, myeloma, leukemialeukemia Thrombocytopenia - bleedingThrombocytopenia - bleeding Anemia - ischemiaAnemia - ischemia –– Including sickle cell anemiaIncluding sickle cell anemia LymphomaLymphoma
- 27. Hyperviscosity effects on retinaHyperviscosity effects on retina
- 28. LeukemiaLeukemia
- 29. LeukemiaLeukemia
- 30. Sickle Cell RetinopathySickle Cell Retinopathy
- 31. Sickle Cell RetinopathySickle Cell Retinopathy
- 32. Endocrine/MetabolicEndocrine/Metabolic Primary disease in this category is:Primary disease in this category is: Diabetes MellitusDiabetes Mellitus
- 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
- 37. NPDRNPDR
- 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
- 41. PDRPDR
- 44. Tractional Retinal DetachmentTractional Retinal Detachment
- 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
- 49. Autoimmune DisordersAutoimmune Disorders Connective tissue diseases -Connective tissue diseases - SLE, SjogrenSLE, Sjogren’’s Syndrome,s Syndrome, Ankylosing SpondylitisAnkylosing Spondylitis GravesGraves’’ diseasedisease Myasthenia gravisMyasthenia gravis Rheumatoid arthritisRheumatoid arthritis Giant cell arteritisGiant cell arteritis
- 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
- 51. Autoimmune SLEAutoimmune SLE Dry eyesDry eyes ScleritisScleritis Peripheral corneal ulcersPeripheral corneal ulcers RetinopathyRetinopathy Optic neuropathyOptic neuropathy
- 53. SLE Optic NeuropathySLE Optic Neuropathy
- 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
- 55. AutoimmuneAutoimmune GravesGraves’’ diseasedisease Manifestations:Manifestations: –– ProptosisProptosis –– Lid retractionLid retraction –– Exposure keratopathyExposure keratopathy –– Strabismus (misaligned eyes)Strabismus (misaligned eyes) –– Optic neuropathyOptic neuropathy
- 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
- 65. AutoimmuneAutoimmune Rheumatoid ArthritisRheumatoid Arthritis Dry eyesDry eyes EpiscleritisEpiscleritis ScleritisScleritis Corneal ulcerationCorneal ulceration UveitisUveitis
- 68. Rheumatoid Necrotizing ScleritisRheumatoid Necrotizing Scleritis
- 69. Rheumatoid Scleromalacia PerforansRheumatoid Scleromalacia Perforans
- 70. Rheumatoid Corneal UlcerationRheumatoid Corneal Ulceration
- 71. Autoimmune Rheumatoid ArthritisAutoimmune Rheumatoid Arthritis Treatment:Treatment: –– Artificial tearsArtificial tears –– Topical steroidsTopical steroids –– Oral steroidsOral steroids –– Immunosuppressive therapyImmunosuppressive therapy Treat in conjunction with a rheumatologistTreat in conjunction with a rheumatologist
- 72. Autoimmune Juvenile RheumatoidAutoimmune Juvenile Rheumatoid ArthritisArthritis Ocular manifestations:Ocular manifestations: –– Asymptomatic iritisAsymptomatic iritis –– Secondary cataracts and glaucomaSecondary cataracts and glaucoma PauciarticularPauciarticular Rheumatoid factor -veRheumatoid factor -ve ANA +ANA +
- 73. Idiopathic Disorders With OcularIdiopathic Disorders With Ocular ManifestationsManifestations SarcoidosisSarcoidosis Multiple SclerosisMultiple Sclerosis HLA B27-associated disorders - ReiterHLA B27-associated disorders - Reiter’’s,s, ankylosing spondylitis, etcankylosing spondylitis, etc BehcetBehcet’’s diseases disease WegenerWegener’’s granulomatosiss granulomatosis
- 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
- 75. Idiopathic SarcoidosisIdiopathic Sarcoidosis Ocular manifestations:Ocular manifestations: –– Orbital and eyelid granulomasOrbital and eyelid granulomas –– Lacrimal gland infiltration - causing dry eyeLacrimal gland infiltration - causing dry eye –– Conjunctival nodulesConjunctival nodules –– Uveitis (intraocular inflammation) - mostUveitis (intraocular inflammation) - most common manifestationcommon manifestation –– Iris nodulesIris nodules –– RetinopathyRetinopathy
- 78. Idiopathic SarcoidosisIdiopathic Sarcoidosis Treatment:Treatment: –– Topical steroidsTopical steroids –– Systemic steroidsSystemic steroids –– Sometimes immunosuppressive therapySometimes immunosuppressive therapy
- 79. Infectious Diseases With OcularInfectious Diseases With Ocular ManifestationsManifestations HIV/AIDSHIV/AIDS Herpes ZosterHerpes Zoster CandidiasisCandidiasis SyphilisSyphilis TBTB Lyme diseaseLyme disease Many othersMany others
- 80. Infectious HIV/AIDSInfectious HIV/AIDS Ocular manifestations:Ocular manifestations: –– Dry eyeDry eye –– KaposiKaposi’’s sarcoma of eyelidss sarcoma of eyelids –– HIV retinopathyHIV retinopathy –– Cytomegalovirus infection (CMV)Cytomegalovirus infection (CMV)
- 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
- 83. HIV/AIDS: CMV RetinitisHIV/AIDS: CMV Retinitis
- 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
- 87. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus Painful, crusty, vesicular lesions alongPainful, crusty, vesicular lesions along distribution of nervedistribution of nerve Exam (of eyes):Exam (of eyes): –– Corneal stromal keratitis (melting)Corneal stromal keratitis (melting) –– UveitisUveitis –– RetinitisRetinitis –– NeuritisNeuritis
- 88. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
- 89. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
- 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
Editor's Notes
- 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
- CD4 Counts &lt; 100 cells/ml: Opportunistic infections (eg. CMV retinitis) &gt; 100 cells/ml: Other ocular infections (eg. syphilis)