Other Eye Conditions Flashcards

1
Q

Amblyopia. What is it?

A

<ul> <li>Poor visual acuity as result of visual deprivation</li> <li>Arises within first years of life</li> <li>Occurs in <a>strabismus</a> (ocular misalignment),anisometropia (unequal refractive errors in eyes), ptosis, corneal or lens opacity</li> <li>Almost always limited to one eye</li> <li>Reversible if detected early</li> <li>Treated by blocking vision in unaffected eye and eliminating provocative condition</li> </ul>

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2
Q

Amblyopia. How does it appear?

A

<ul><li>Subnormal visual acuity in one eye</li> <li>One of provocative conditions (strabismus, anisometropia, ptosis, media opacity) will be present but may not be obvious </li><li>No afferent pupil defect </li><li>No other ocular or retro-ocular abnormalities to account for subnormal acuity</li></ul>

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3
Q

Amblyopia. What else looks like it?

A

<ul><li>Uncorrected refractive error</li> <li>Lesion of ocular media, retina, or visual pathway</li><li>Psychogenic visual loss</li></ul>

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4
Q

Amblyopia. How do you manage it?

A

<ul><li>Refer non-urgently for diagnosis of provocative condition and treatment</li></ul>

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5
Q

Amblyopia. What will happen?

A

<ul><li>Treatment consists of occlusion or cycloplegia of unaffected eye and elimination of provocative condition</li><li>Reversal of amblyopia most effective if treatment undertaken at early age</li> </ul>

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6
Q

Basal Cell Carcinoma. What is it?

A

<ul><li>Most common malignant tumor of lid</li><li>Does not metastasize, but can burrow deep into orbit </li></ul>

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7
Q

Basal Cell Carcinoma. How does it appear?

A

<ul> <li>Slowly <a>enlarging lump</a> or plaque </li><li>Most often on lower lid </li></ul>

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8
Q

Basal Cell Carcinoma. What else looks like it?

A

<ul><li>Squamous carcinoma, sebaceous carcinoma, seborrheic keratosis, wart, chalazion, polyp, keratoacanthoma, skin tag, cutaneous horn, cyst, xanthelasma, nevus, malignant melanoma, Kaposi sarcoma</li></ul>

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9
Q

Basal Cell Carcinoma. How do you manage it?

A

<ul><li>Realize that malignant and benign lid lesions cannot be distinguished by their appearance, so...</li><li>Refer patients non-urgently for any persistent lump or deformity of lid </li><li>Refer patients more urgently if lump is growing</li></ul>

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10
Q

Basal Cell Carcinoma. What will happen?

A

<ul><li>Any suspicious lesion will undergo biopsy</li><li>Early detection helps because penetrating lesions need large excisions that may affect appearance and even eye function</li> </ul>

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11
Q

Cataract. What is it?

A

<ul><li>Opacification of eye’s crystalline lens</li><li>Called "cataract" by Greek physicians who thought it looked like a waterfall</li><li>Caused by aging degeneration of lens protein</li><li>Also caused by intraocular inflammation, trauma, metabolic and hereditary disorders</li></ul>

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12
Q

Cataract. How does it appear?

A

<ul><li>Patient reports slowly progressive blurred vision in affected eye</li><li>Vision often improves with pinhole</li> <li><a>Early cataract</a> visible with slit lamp biomicroscope as golden, gray, black discoloration of lens </li><li>Advanced cataract visible with ophthalmoscope as loss of "red reflex" in pupil</li> </ul>

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13
Q

Cataract. What else looks like it?

A

<ul> <li>Uncorrected refractive error, corneal, retinal, and visual pathway lesions</li> <li>Dense cataracts, which make pupil look gray or white, are mimicked by vitreous and retinal lesions</li> </ul>

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14
Q

Cataract. How do you manage it?

A

<ul><li>Refer non-urgently</li></ul>

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15
Q

Cataract. What will happen?

A

<ul> <li>Cataracts are removed surgically through small incisions and ultrasonic fragmentation </li> <li>Posterior lens capsule left behind</li> <li><a>Plastic lens implant</a> inserted in place of extracted crystalline lens</li> <li>Surgical procedure takes less than 30 minutes and is painless </li> <li>Visual recovery prompt and full in 99% of eyes provided no other reason for subnormal sight</li><li>Posterior lens capsule remnant may opacify and require laser treatment</li></ul>

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16
Q

Central Retinal Artery Occlusion. What is it?

A

<ul><li>Infarction of retina</li><li>Caused by thrombotic or embolic occlusion of retinal arteries</li> <li>Sources of thrombosis are systemic hypertension, dyslipidemia, hypercoagulable states</li><li>Sources of embolism are atheromas of cervical carotid bifurcation or abnormalities of cardiac valves, wall, or rhythm </li></ul>

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17
Q

Central Retinal Artery Occlusion. How does it appear?

A

<ul><li>Sudden painless loss of vision usually confined to one eye</li><li>Afferent pupil defect in affected eye </li> <li><a>Milky appearance of retina</a> because ischemic swelling causes loss of its transparency</li> <li><a>Cherry-red spot in fovea</a> (spared because it is nourished by choroidal rather than retinal arteries)</li></ul>

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18
Q

Central Retinal Artery Occlusion. What else looks like it?

A

<ul><li>Nothing, but...</li> <li>Distinctive milky white retina with cherry red spot may not develop for first 24 hours</li> </ul>

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19
Q

Central Retinal Artery Occlusion. How do you manage it?

A

<ul><li>Consider this diagnosis in patient with sudden monocular persistent loss of vision especially if afferent pupil defect present</li><li>Refer emergently to ophthalmologist or emergency room</li></ul>

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20
Q

Central Retinal Artery Occlusion. What will happen?

A

<ul><li>No effective treatment (including thrombolysis, anticoagulation), but...</li> <li>Patient needs evaluation for stroke-prone state</li> <li>Some vision may return spontaneously</li> </ul>

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21
Q

Central Retinal Vein Occlusions. What is it?

A

<ul> <li>Blockage of flow in vein that drains inner retina</li> <li>Common causes: systemic hypertension, diabetes, arteriosclerosis, hypercoagulable states</li> </ul>

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22
Q

Central Retinal Vein Occlusions. How does it appear?

A

<ul><li>Patient reports acute or subacute monocular vision loss, sometimes with flickering ("scintillations")</li><li>Flame-shaped hemorrhages originating around optic disc and extending along branches of central retinal vein</li><li>Distended retinal veins</li><li><a>Cotton wool spots</a></li><li><a>Hard exudates</a></li></ul>

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23
Q

Central Retinal Vein Occlusions. What else looks like it?

A

<ul> <li>Retinal hemorrhages associated with sudden increase in intracranial pressure (<a>Terson syndrome</a>) </li> <li>Thrombocytopenia and other blood dyscrasias </li> <li><a>Papilledema</a></li> <li>Hemorrhagic optic neuritis (papillitis)</li> <li>Traumatic avulsion of optic nerve</li> <li>Hemorrhagic retinitis associated with herpesviruses</li> <li><a>Carotid-cavernous arteriovenous fistula</a></li> <li>Cavernous sinus thrombosis</li> </ul>

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24
Q

Central Retinal Vein Occlusions. How do you manage it?

A

<ul> <li>Refer to ophthalmologist urgently</li> </ul>

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25
Q

Central Retinal Vein Occlusions. What will happen?

A

<ul><li>No immediate treatment (anticoagulation not used) </li><li>Blood eventually absorbed, but...</li><li>Recovery of vision depends on severity of retinal ischemia </li><li><a>New blood vessels</a> may appear within months on iris surface ("iris neovascularization"), which is well seen on <a>iris angiogram</a> (compare to <a>normal iris angiogram</a>)</li><li>Iris neovascularization zippers up anterior chamber angle structures, impedes flow of aqueous, and greatly elevates intraocular pressure ("neovascular glaucoma")</li><li>Neovascular glaucoma causes severe pain, further loss of vision </li><li>Pan-retinal photocoagulation, intraocular injection of anti-vascular endothelial growth factor agents may reverse this process</li></ul>

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26
Q

Choroidal Melanoma. What is it?

A

<ul><li> Malignant melanoma arising in choroid </li> <li> Arises de novo or from transformation of nevi </li> <li> Most common primary intraocular tumor in adults, but... </li> <li> Only 0.5 per 100,000 diagnosed yearly in United States </li> <li> Age at diagnosis is 40-75 years, peaking at age 50 </li> <li> 5-year survival ranges from 55% to 80% even with treatment </li> </ul>

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27
Q

Choroidal Melanoma. How does it appear?

A

<ul> <li><a>Mound</a> that often lifts retina, as seen here on <a>optical coherence tomography</a> (OCT)</li> <li>Disturbs vision if located under fovea; otherwise may be asymptomatic</li> <li>Pigmentation ranges from yellow to black</li> <li>May be hard to recognize if <a>lightly pigmented</a></li></ul>

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28
Q

Choroidal Melanoma. What else looks like it?

A

<ul> <li><a>Choroidal nevus</a></li> <li><a>Retinal pigment epithelial hypertrophy</a></li> <li><a>Choroidal inflammation </a></li><li><a>Choroidal metastasis</a></li><li><a>Retinal detachment</a></li> </ul>

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29
Q

Choroidal Melanoma. How do you manage it?

A

<ul> <li>Refer any patient with new vision loss with urgency depending on symptoms</li> <li>Refer non-urgently any patient with an incidentally-noted lesion in the retina or choroid </li> </ul>

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30
Q

Choroidal Melanoma. What will happen?

A

<ul> <li>Presumptive diagnosis of choroidal melanoma can be made accurately with combination of ophthalmoscopy, ultrasound, optical coherence tomography, and fluorescein angiography</li> <li>Depending on size and location of lesion, treatment will involve radiotherapy or enucleation </li> <li>No rigorous evidence that treatment of any kind alters survival</li> </ul>

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31
Q

Congenital Glaucoma. What is it?

A

<ul><li><a>Malformed trabecular meshwork</a> at birth causes elevated intraocular pressure, enlarged eye, cloudy cornea, tearing</li> <li>Surgery to repair meshworkor <a>bypass it</a> and lower intraocular pressure must be prompt to prevent permanent vision loss.</li> </ul>

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32
Q

Congenital Glaucoma. How does it appear?

A

<ul> <li>Fussy baby, cloudy cornea, tearing, enlarged eye ("buphthalmos", or ox eye)</li> <li>May be monocular or binocular</li> <li>Elevated intraocular pressure can be measured</li> <li>Usually not associated with other congenital anomalies</li> </ul>

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33
Q

Congenital Glaucoma. What else looks like it?

A

<ul> <li><a>Congenital corneal dysplasias</a> or systemic metabolic disorders causing cloudy corneas, but...</li> <li>They usually do not have elevated intraocular pressure, large eye, or tearing</li> </ul>

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34
Q

Congenital Glaucoma. How do you manage it?

A

<ul> <li>Refer urgently any baby with cloudy cornea</li> </ul>

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35
Q

Congenital Glaucoma. What will happen?

A

<ul><li>Eye surgery to repair or <a>bypass trabecular meshwork</a></li> <li>Visual outcome usually favorable, especially if detection is prompt!</li> </ul>

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36
Q

Dry Age-related Macular

A

<ul><li>Aging degeneration of the retinal pigment epithelium in fovea</li><li>Most common cause of persistent vision loss in elderly adults in advanced industrial countries</li><li>Cause unknown</li><li>Smoking may accelerate progression</li> <li>Oral intake of special combination of vitamins slows progression in some cases</li></ul>

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37
Q

Dry Age-related Macular

A

<ul> <li>Starts with <a>yellow-white discoloration of macular region</a> owing to atrophy of retinal pigment epithelium</li> <li>Discrete round yellow-white patches called "<a>retinal drusen</a>" often visible</li></ul>

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38
Q

Dry Age-related Macular

A

<ul><li><a>Other yellow white things in retina</a></li></ul>

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39
Q

Dry Age-related Macular

A

<ul> <li>Refer non-urgently if this is incidental finding</li> <li>Refer urgently if the patient has new vision loss</li> </ul>

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40
Q

Dry Age-related Macular

A

<ul> <li>Over time, drusen often increase (<a>Watch this typical sequence</a>)</li> <li>In worst cases, <a>large areas of retinal atrophy</a> appear and visual acuity declines</li> <li>For dry age-related macular degeneration with large drusen, combination of vitamin C 500mg, vitamin E 400 IU, zinc oxide 80mg, cupric oxide 2mg, lutein 10mg, and zeaxanthin 2mg reduces progression of vision loss </li> <li>Smokers will be advised to quit</li> <li>Patients will be advised to test themselves periodically with Snellen near vision card and Amsler grid to detect drop in vision or perceived distortion of grid lines (<a>"metamorphopsia"</a>), which might signal that...</li> <li>New blood vessels have grown from choroid into submacular retina ("subretinal neovascularization"), which has led to... </li> <li><a>Bleeding under the retina</a> that further blurs and distorts vision (<a>Wet age-related macular degeneration</a>)</li> <li>Periodic injections of vascular endothelial growth factor (VEGF) inhbitors into vitreous cavity (yes, really!) slow and sometimes reverse vision loss caused by exudate and bleeding into fovea</li> </ul>

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41
Q

Idiopathic Orbital Inflammation. What is it?

A

<ul><li>Autoimmune inflammation of orbital soft tissues ("idiopathic orbital inflammation," abbreviated IOI)</li> <li>Inflammation often seated in extraocular muscles and then also called "orbital myositis"</li> <li>Diagnosis based on clinical features, imaging, and sometimes biopsy</li><li>Usually improves with systemic or orbital injection of corticosteroids, but...</li> <li>May recur</li> </ul>

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42
Q

Idiopathic Orbital Inflammation. How does it appear?

A

<ul><li>Periocular pain, lid swelling, <a>eye surface vessel hyperemia</a>, diplopia</li> <li>Usually unilateral</li> <li>Onset subacute</li> <li>Orbital imaging may show proptosis, lid swelling, vascular congestion, extraocular muscle or lacrimal gland enlargement, dural and periosteal enhancement</li> </ul>

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43
Q

Idiopathic Orbital Inflammation. What else looks like it?

A

<ul> <li>Orbital inflammation caused by <a>granulomatous polyangiitis</a>, other vasculitides, connective tissue diseases, sarcoidosis, fungal infection, all of which require non-orbital findings or biopsy for diagnosis </li> <li><a>Graves disease</a>, but IOI has more rapid onset, more pain, is more often unilateral, and has no lid retraction or lag </li> <li><a>Bacterial orbital cellulitis</a>, but IOI has slower onset, and is more likely to show extraocular muscle or lacrimal gland enlargement</li> <li><a>Orbital tumor</a>, but imaging in IOI does not show masses except within extraocular muscles or lacrimal gland</li> <li><a>Cavernous sinus arteriovenous fistula</a>, but that shows enlarged superior ophthalmic vein on imaging</li></ul>

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44
Q

Idiopathic Orbital Inflammation. How do you manage it?

A

<ul> <li>Refer patient urgently for clinical and imaging assessment</li> </ul>

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45
Q

Idiopathic Orbital Inflammation. What will happen?

A

<ul> <li>Prompt orbital imaging (CT or MRI) necessary for diagnosis</li> <li>If imaging suggests IOI, next step is CT of chest, abdomen, pelvis to rule out other sites of inflammation or tumor</li> <li>If orbit only site of disease, patient will be treated with corticosteroids, with expected improvement within days</li> <li>If there is no improvement or recurrence upon tapering steroids, orbital biopsy will be considered to exclude non-idiopathic inflammation, neoplasm</li> <li>IOI may resolve without treatment or after one episode of treatment, but...</li> <li>May also be recurrent, requiring chronic immunomodulatory treatment, and...</li> <li>Leaving behind scarred tissue that causes permanent diplopia and even vision loss </li></ul>

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46
Q

Iris Melanoma. What is it?

A

<ul> <li> Brown pigmented mass on iris </li> <li>Low-grade malignancy</li> <li>Not associated with melanoma of skin or other tissues</li> </ul>

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47
Q

Iris Melanoma. How does it appear?

A

<ul><li><a>Brown plaque on iris surface</a></li> <li>Pupil may be distorted</li> </ul>

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48
Q

Iris Melanoma. What else looks like it?

A

<ul> <li>Iris freckle—layer of melanocytes present at birth and not enlarging</li> <li><a>Iris nevus</a>—mounds of melanocytes present at birth and not enlarging very much</li> <li>Lisch nodule—small light brown non-enlarging hamartomas found in <a>neurofibromatosis type 1</a> </li> <li>Granuloma of sarcoidosis—inflammatory mound located at iris margin or mid-iris region</li> </ul>

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49
Q

Iris Melanoma. How do you manage it?

A

<ul> <li>Refer non-urgently if patient has new visual symptoms or thinks lesion new or growing</li> </ul>

50
Q

Iris Melanoma. What will happen?

A

<ul> <li>Lesion suspicious for melanoma will be biopsied</li> <li>Metastasis very rare unless lesion extends into ciliary body</li> </ul>

51
Q

Non-arteritic Ischemic Optic

A

<ul><li>Sudden loss of vision caused by infarction of optic nerve</li><li>Affects adults aged over 45 years </li><li>Associated with diabetes, systemic hypertension, smoking, dyslipidemia, family history of arteriosclerosis or drop in systemic blood pressure </li> <li> Called "non-arteritic" to distinguish it from ischemic optic neuropathy associated with <a>giant cell arteritis</a> and other arteritides </li><li>Visual loss mild to severe and largely irreversible</li><li>No effective treatment </li> </ul>

52
Q

Non-arteritic Ischemic Optic

A

<ul><li>Optic disc <a>usually swollen</a> in acute phase and pale in chronic phase </li><li>Usually monocular </li> <li>Visual acuity may be normal but visual field loss always present </li><li>Afferent pupil defect on affected side</li><li>No pain or other symptoms </li><li>Onset often upon awakening </li><li>Often history of aggressively treated systemic hypertension </li> </ul>

53
Q

Non-arteritic Ischemic Optic

A

<ul> <li>Arteritic ischemic optic neuropathy in <a>giant cell arteritis</a>, but that is usually accompanied by headache, jaw pain provoked by chewing ("jaw claudication"), limb girdle joint pain, fatigue, malaise, low-grade fever, and elevated sedimentation rate and/or C-reactive protein </li> <li><a>Optic neuritis</a>, usually occurring in younger patients </li> <li><a>Papilledema</a>, usually binocular with relatively preserved vision </li> <li>Neoplastic optic neuropathy, usually with previously known cancer </li> </ul>

54
Q

Non-arteritic Ischemic Optic

A

<ul><li>Refer urgently to ophthalmologist because of concern for arteritic ischemic optic neuropathy in giant cell arteritis</li> </ul>

55
Q

Non-arteritic Ischemic Optic

A

<ul> <li>Visual loss may progress over 14 days, largely irreversible, but often mild </li> <li>Similar process may affect other eye in 10% to 15% of patients within 10 years </li> <li>Best way to reduce second-eye involvement is to address arteriosclerotic risk factors and avoid aggressive lowering of systemic blood pressure </li> </ul>

56
Q

Open-Angle Glaucoma. What is it?

A

<ul><li>Slowly progressive cupping of optic disc leading to vision loss</li> <li>Often first detected by finding pathologic optic disc cupping on screening exams</li> <li>Causes still undefined but elevated ocular pressure contributes</li> <li>Intraocular pressure often elevated because <a>aqueous fluid does not flow out normally through trabecular meshwork</a></li> <li>Treated by lowering intraocular pressure with topical medications or with eye surgery that diverts aqueous through <a>hole in sclera</a></li> <li>Accounts for over 95% of glaucoma cases</li> <li>Affects about 1% of adults aged over 40 years</li> <li>Family history of open-angle glaucoma in 20% </li> </ul>

57
Q

Open-Angle Glaucoma. How does it appear?

A

<ul><li>Most afflicted patients are asymptomatic until vision loss is far advanced</li> <li><a>Pathologic cupping of optic disc</a> is earliest sign; compare to <a>normal disc</a> which has cup-to-disc ratio of 0.5 or less</li><li>Visual field defect if condition advanced </li><li>Elevated intraocular pressure in many-but not all!</li></ul>

58
Q

Open-Angle Glaucoma. What else looks like it?

A

<ul> <li>Other optic neuropathies and retinopathies, but pathologic cupping of optic disc almost unique to glaucoma</li> <li>"Secondary glaucoma," caused by elevated intraocular pressure in patients with iritis, hyphema, or other eye trauma</li> <li><a>Coloboma of optic disc</a></li> <li><a>Tilted disc of myopia</a></li> <li>Non-glaucomatous (arteritic ischemic and compressive) optic neuropathies (but pathologic cupping rare)</li></ul>

59
Q

Open-Angle Glaucoma. How do you manage it?

A

<ul> <li>Screen for this condition by looking for pathologic optic disc cupping in adults, especially those with family history of glaucoma, noting that...</li> <li>Normal ratio of physiologic cup diameter to optic disc diameter should not exceed 0.5 </li> <li>If you think optic disc is pathologically cupped, refer non-urgently for confirmation and management</li><li>Ophthalmoscopic screening for optic disc cupping is critical, especially in those with family history of open-angle glaucoma </li> <li>Screening by measuring intraocular pressure (tonometry) not effective because intraocular pressure often not elevated in open-angle glaucoma AND...</li><li>Measuring intraocular pressure takes practice and skill</li></ul>

60
Q

Open-Angle Glaucoma. What will happen?

A

<ul> <li>Eyedrops used to lower intraocular pressure</li> <li>If eyedrops fail to lower pressure, or optic disc cupping and vision loss progress, surgical treatment may be used, consisting of....</li> <li><a>Making a hole in sclera</a> to allow aqueous to bypass trabecular meshwork </li> <li>Medical and surgical treatment not always successful in halting progression of glaucoma, so that....</li> <li>Some patients become visually disabled, but...</li> <li>Early treatment considered beneficial</li> </ul>

61
Q

Optic Neuritis. What is it?

A

<ul><li>Inflammation of optic nerve causing vision loss </li><li>Usually affects patients younger than 50 years</li><li>May be part of multiple sclerosis, other autoimmune disorders, or infections</li></ul>

62
Q

Optic Neuritis. How does it appear?

A

<ul><li>Acute or subacute vision loss, usually monocular</li> <li>Often periocular pain made worse with eye movement</li> <li>Sometimes optic disc swollen, but fundus exam often normal</li><li><a>Afferent pupil defect</a> usually present</li> <li><a>Enhancement (bright signal) of affected optic nerve with MRI contrast agent</a>, and sometimes...</li><li>High signal abnormalities elsewhere in brain that reflect <a>multifocal demyelination</a></li> </ul>

63
Q

Optic Neuritis. What else looks like it?

A

<ul><li>Retinopathies and other optic neuropathies</li> <li>Retrobulbar visual pathway disease</li> <li><a>Psychogenic visual loss</a></li> </ul>

64
Q

Optic Neuritis. How do you manage it?

A

<ul> <li>Refer urgently any patient with acute or subacute vision loss </li> </ul>

65
Q

Optic Neuritis. What will happen?

A

<ul><li>In primary demyelinating optic neuritis, high-dose intravenous methylprednisolone 1 gm for 3 days followed by oral prednisone 1 mg/kg for 11 days slightly hastens recovery, but...</li> <li>Spontaneous total or near total visual recovery occurs in 85%, and...</li> <li>Corticosteroid treatment does not affect final visual outcome or long term incidence of multiple sclerosis</li> <li>In optic neuritis associated with other autoimmune disorders, corticosteroid treatment may be very effective</li> <li>In optic neuritis associated with infections, treatment directed at those infections </li> </ul>

66
Q

Psychogenic Visual Loss. What is it?

A

<ul><li>Patient denies sight yet examination strongly suggests that sight is intact</li><li>Can be monocular or binocular, transient or persistent, central or peripheral, acute or chronic</li><li>May be psychiatric or behavioral disturbance (anxiety, depression, somatoform disorder, hypochondriasis, conversion, malingering)</li> <li>Common in children who aim for attention or to avoid stresses</li><li>Often isolated deficit </li><li>May be difficult to distinguish from organic visual loss</li> <li>Sometimes psychogenic and organic visual loss coexist ("embellishment") </li> </ul>

67
Q

Psychogenic Visual Loss. How does it appear?

A

<ul><li>Most commonly as persistent monocular profound visual loss</li> <li>Less commonly as homonymous hemianopia, bitemporal hemianopia, monocular temporal hemianopia </li> <li>Clues to psychogenic nature of visual loss are vague history of onset, inconsistent or bizarre responses on vision testing, normal pupil function and ocular structures, known psychiatric or behavior disorder</li><li>Malingerers aim for gain—compensation, relief from work or other obligations</li><li>Somatizers aim to resolve depression, psychosocial conflicts or predicaments</li><li>Hypochondriacs convinced they are ill</li><li>Conversion hysterics trying to avoid deep psychic issues </li> </ul>

68
Q

Psychogenic Visual Loss. What else looks like it?

A

<ul> <li>Organic visual loss, which can be difficult to exclude</li> </ul>

69
Q

Psychogenic Visual Loss. How do you manage it?

A

<ul> <li>Refer to ophthalmologist who should have skills and tricks to unmask this condition</li> </ul>

70
Q

Psychogenic Visual Loss. What will happen?

A

<ul> <li>If issue can be identified and resolved, symptom often resolves </li> <li>Malingerers often hold fast and may be confrontative and even dangerous</li> <li>Underlying issues in children usually easier to identify, although abuse must be excluded</li> </ul>

71
Q

Refractive Disorders. What is it?

A

<ul> <li>Eyes with refractive errors cannot focus viewed objects clearly on retina, unlike...</li> <li><a>Eyes without refractive errors</a> which can focus light rays onto retina</li> <li><a>Myopic eyes</a> have excessive refractive power so that they focus far away objects <em>in front of the retina</em></li> <li><a>Hyperopic eyes</a> have insufficient refractive power so that they focus far away objects <em>behind the retina</em></li> <li><a>Astigmatic eyes</a> have uneven corneal curvature so that they <em>cannot produce a point focus on the retina</em><em></em></li> <li><a>Presbyopic eyes</a> have lost their ability to increase focusing power for objects viewed at reading distance (accommodation)</li></ul>

72
Q

Refractive Disorders. How does it appear?

A

<ul> <li>Blurred vision that often clears with squinting or looking through pinhole </li> <li>Patients with myopia have blurred vision for objects viewed far away</li> <li>Patients with hyperopia have blurred vision mostly for objects viewed nearby</li> <li>Patients with astigmatism have blurred vision for objects viewed at any distance</li> <li>Patients with presbyopia have blurred vision for objects viewed at reading distance</li> </ul>

73
Q

Refractive Disorders. What else looks like it?

A

<ul> <li>Lesions of the ocular media, retina, and visual pathway </li> </ul>

74
Q

Refractive Disorders. How do you manage it?

A

<ul><li>Refer to vision care providers, who are able to detect and correct refractive errors and distinguish them from other causes of impaired vision</li></ul>

75
Q

Refractive Disorders. What will happen?

A

<ul> <li>Nearly all refractive errors can be corrected with spectacles or contact lenses, or by surgically reshaping cornea</li> <li><a>Myopia is corrected</a> with a spherical concave lens that moves the focus backwards in the eye so that it falls onto the retina</li> <li><a>Hyperopia is corrected</a> with a spherical convex lens that moves the focus forward onto the retina</li> <li><a>Astigmatism is corrected</a> with a cylindrical lens, which has more focusing power in one axis than another</li> <li>Presbyopia does not appear until after age 40; before then, the lens is flexible enough so that contraction of the ciliary muscle allows it to assume a convex front surface and focus objects viewed at reading distance; after age 40, the lens proteins gradually degenerate, the lens stiffens, and will not round up to allow focusing of near objects on the retina</li> <li><a>Presbyopia is corrected</a> by placing a convex lens in front of the eye. Because it is used only for seeing near objects, it is prescribed either as a half-glass or as the bottom part of a bifocal if the patient needs a correction for distance viewing</li></ul>

76
Q

Retinal Break. What is it?

A

<ul><li><a>Hole</a> in neurosensory part of retina causes it to separate from underlying retinal pigment epithelium </li><li>Usually results from <a>tugging by vitreous</a></li><li>Common causes are eye trauma (including intraocular surgery), high myopia, intraocular inflammation, diabetes, and aging </li> <li><a>Can lead to retinal detachment</a></li> </ul>

77
Q

Retinal Break. How does it appear?

A

<ul><li>May be asymptomatic, or...</li><li>Patient reports sudden onset of flashes and/or floaters</li><li>Hole in retinal periphery usually not seen with direct ophthalmoscopy and even hard to detect with indirect ophthalmoscopy</li></ul>

78
Q

Retinal Break. What else looks like it?

A

<ul> <li>Vitreous tug on retina without retinal break</li> <li><a>Vitreous separation</a> from retina without retinal break</li> </ul>

79
Q

Retinal Break. How do you manage it?

A

<ul> <li>Refer urgently patient with new-onset flashes or floaters</li> </ul>

80
Q

Retinal Break. What will happen?

A

<ul> <li>Retinal break may need to be repaired to prevent retinal detachment</li> </ul>

81
Q

Retinal Detachment. What is it?

A

<ul> <li>Separation of a segment of neurosensory retina from underlying retinal pigment epithelium, causing vision loss </li> <li><a>Retinal break</a> allows liquid vitreous to seep between retinal layers to cause <a>retinal detachment</a></li> <li>Predisposing conditions are eye trauma (including intraocular surgery), high myopia, intraocular inflammation, and aging</li> </ul>

82
Q

Retinal Detachment. How does it appear?

A

<ul> <li>Patients often report sudden onset of flashes, floaters, and visual field loss, but...</li> <li>Symptoms may be subtle, subacute, or altogether absent </li> <li>Ophthalmoscopy reveals <a>billowy folds</a> of detached retina, although...</li> <li>Detached retina usually not visible without special instruments, and...</li> <li>Some detachments are shallow and difficult to see even by experts </li> </ul>

83
Q

Retinal Detachment. What else looks like it?

A

<ul> <li><a>Retinal break</a></li> <li><a>Vitreous detachment</a></li> <li>Other retinopathies</li> </ul>

84
Q

Retinal Detachment. How do you manage it?

A

<ul> <li>Refer urgently any patient with symptoms suggesting retinal detachment</li> </ul>

85
Q

Retinal Detachment. What will happen?

A

<ul> <li>Retinal detachment must be repaired surgically</li> <li>Visual prognosis better if detachment has not spread to foveal region, therefore...</li> <li>Premium on early diagnosis and referral</li> </ul>

86
Q

Retinoblastoma. What is it?

A

<ul> <li>Most common intraocular tumor of childhood </li> <li>1 in every 18,000 births </li> <li>Up to 500 new cases diagnosed each year in United States</li> <li>Diagnosed usually at birth or within few years of life</li> <li>Less than 10% have family history of retinoblastoma</li> <li>Risk of death in untreated cases nearly 100%</li> <li>Early diagnosis and treatment of small tumors lead to best outcomes</li> </ul>

87
Q

Retinoblastoma. How does it appear?

A

<ul> <li><a>White (cat’s eye) pupil</a>, also called leukocoria, if tumor large and near back of lens</li> <li>Smaller tumors visible only on ophthalmoscopy</li> <li>Many young children present with poor vision or misaligned eyes (<a>strabismus</a>)</li> </ul>

88
Q

Retinoblastoma. What else looks like it?

A

<ul> <li>Leukocoria also caused by many other vitreoretinal disorders, usually separable from retinoblastoma by ophthalmoscopy, ultrasound, optical coherence tomography, CT, MRI</li> </ul>

89
Q

Retinoblastoma. How do you manage it?

A

<ul> <li>Check for leukocoria and strabismus in babies and screen for subnormal vision in young children</li> <li>Refer suspicious cases within weeks</li> </ul>

90
Q

Retinoblastoma. What will happen?

A

<ul> <li>Cryo, laser, radiation, and chemotherapy provide 30% to 90% cure depending on pre-treatment extent of tumor </li> <li>Enucleation is performed for very large tumors or eyes with very poor sight</li> <li>Genetic counseling is critical as transmissibility is complex issue</li> </ul>

91
Q

Retinopathy of Prematurity. What is it?

A

<ul> <li>Fibrovascular proliferation in retina of pre-term infants </li> <li> Cause is premature exposure to extra-uterine environment rich in oxygen </li> <li> Occurs in 80% of neonates weighing less than 1000gm and in 20% weighing between 1000gm and 1250gm </li> <li> Pathology develops first in peripheral retina at 30 to 45 weeks of postmenstrual age and often regresses spontaneously, but... </li> <li> <a>Retinal detachment</a> is feared complication </li> </ul>

92
Q

Retinopathy of Prematurity. How does it appear?

A

<ul><li>Earliest sign is zone of avascularity in far peripheral retina that can be detected only with skilled indirect ophthalmoscopy</li><li>In advanced disease, fibrovascular proliferation may extend to optic disc and drag it ("<a>dragged disc</a>")</li> </ul>

93
Q

Retinopathy of Prematurity. What else looks like it?

A

<ul> <li>Nothing, but...</li> <li>Challenge is to recognize subtle early signs so that...</li> <li>Baby can be examined frequently to detect dangerous progression</li> </ul>

94
Q

Retinopathy of Prematurity. How do you manage it?

A

<ul><li>Arrange for at-risk babies to be examined at about 4 weeks after birth by ophthalmologist skilled in screening for this condition</li></ul>

95
Q

Retinopathy of Prematurity. What will happen?

A

<ul> <li>Screening examinations will continue until retinal vessels have grown out to retinal periphery such that retinopathy will not occur</li> <li>Most retinopathy of prematurity regresses spontaneously, but when signs of dangerous progression are found...</li> <li>Treatment consists of laser photocoagulation, shown to be effective in reducing vision loss</li> </ul>

96
Q

Strabismus. What is it?

A

<ul> <li>Ocular misalignment, especially with onset at birth or in childhood </li> <li>May reflect disorder of brain, cranial nerves, neuromuscular junction, or extraocular muscles</li> <li>Diagnosis based on history, pattern of misalignment, and associated findings</li> </ul>

97
Q

Strabismus. How does it appear?

A

<ul><li>Patient reports <a>diplopia</a> that disappears upon covering either eye, but remember that...</li> <li>Children rarely report diplopia because they suppress image from deviating eye</li> <li>One eye appears not to be fixating stationary viewed object </li> <li>One eye appears not to be tracking moving viewed object</li> <li>One eye appears not to be moving fully in one or more gaze directions </li> <li>Covering one eye ("<a>cover test</a>") elicits fixational movement by other eye</li> </ul>

98
Q

Strabismus. What else looks like it?

A

<ul> <li>Wide nasal bridge gives false impression of convergent strabismus ("pseudostrabismus")</li> <li><a>Displacement of an eye by orbital tumor</a> or trauma may give false impression of misalignment </li><li>Ptosis or lid retraction may give false impression of misalignment</li> </ul>

99
Q

Strabismus. How do you manage it?

A

<ul> <li>Confirm strabismus by performing cover test and eliciting fixational eye movement, or...</li> <li>Noting if diplopia disappears as patient covers either eye</li> <li>Understand that strabismus may be hard to diagnose if misalignment is small, patient does not report diplopia, is uncooperative, or cannot properly execute fixation movement on cover test, so...</li> <li>If you are not sure of your test results or patient reports diplopia... </li> <li>Refer with urgency that depends on how recently strabismus was noted and on accompanying pertinent findings, because...</li> <li>Brain aneurysm or other life-threatening conditions could be present</li> </ul>

100
Q

Strabismus. What will happen?

A

<ul><li>Strabismus in early childhood often accompanied by <a>amblyopia</a>, which must be promptly treated to prevent persistent vision loss </li><li>Treatment of strabismus depends on underlying cause</li> <li>Causes in young children are excessive convergence of brain stem origin ("congenital esotropia"), esotropia of hyperopia ("accommodative esotropia"), impaired vision ("sensory strabismus"), and excessive idiopathic divergence ("exotropia")</li><li>Causes in adults are internuclear ophthalmoplegia, skew deviation, cranial nerve palsies, myasthenia gravis, extraocular muscle inflammation, and orbital trauma</li><li>Most urgent diagnosis is <a>third cranial nerve palsy</a> because could be caused by brain aneurysm with imminent rupture and death </li></ul>

101
Q

Tonic Pupil. What is it?

A

<ul><li>Dilated pupil caused by lesion of ciliary ganglion or nerves</li> <li>Part of limited post-viral or idiopathic dysautonomia</li> <li>May also result from orbital surgery</li> <li>Often misdiagnosed as partial third cranial nerve palsy</li> </ul>

102
Q

Tonic Pupil. How does it appear?

A

<ul> <li>Dilated pupil that does not constrict to bright light, constricts slowly to target fixated at close range, and dilates slowly upon refixation on distant target</li> <li>Slit lamp examination often shows that pupil constricts segmentally (stromal streaming)</li> <li>Accommodation may be impaired in affected eye</li> <li>Deep tendon reflexes may be absent</li> </ul>

103
Q

Tonic Pupil. What else looks like it?

A

<ul> <li>Iris damage from trauma, intraocular surgery, inflammation</li> <li>Accidental or deliberate ocular instillation of anticholinergic substances</li> </ul>

104
Q

Tonic Pupil. How do you manage it?

A

<ul> <li>Do not refer patient to emergency room for unilaterally dilated pupil unless ptosis, diplopia, or eye movement abnormality present</li> <li>Refer to ophthalmologist non-urgently to confirm diagnosis of tonic pupil </li> </ul>

105
Q

Tonic Pupil. What will happen?

A

<ul> <li>Life-long condition but does not cause troublesome symptoms</li> <li>Affected pupil often becomes smaller than unaffected pupil</li> <li>No related medical problems will emerge, but...</li> <li>Pupil of other eye may later become similarly affected</li> <li>Refer patient emergently to ophthalmologist or emergency room if you find upper lid ptosis and miosis, especially if acute and accompanied by new neck pain or diplopia</li> </ul>

106
Q

Visual Pathway Disorder. What is it?

A

<ul><li>Damage to the visual pathway somewhere between optic nerve and visual cortex, including optic chiasm, optic tract, and optic radiations</li> <li>Site of damage often localizable by ophthalmoscopy, pupil reactions, and pattern of visual field defects</li> </ul>

107
Q

Visual Pathway Disorder. How does it appear?

A

<ul><li>Patients may report monocular or binocular blurred, blank, dim, dark, or sparkling vision</li> <li>Optic nerve damage may be accompanied by swollen optic disc</li> <li>Unilateral or asymmetric optic nerve damage produces <a>afferent pupil defect</a></li> <li>Lesions of optic nerve produce nerve fiber bundle visual field defects</li> <li>Lesions of optic chiasm usually produce bitemporal hemianopias</li> <li>Lesions of optic tracts, optic radiations, and visual cortex usually produce homonymous hemianopias</li> <li><a>See patterns of visual field loss</a> and how they localize lesions of visual pathway </li> </ul>

108
Q

Visual Pathway Disorder. What else looks like it?

A

<ul> <li>Undetected <a>refractive error</a></li> <li>Subtle ocular media abnormalities</li> <li>Subtle retinal abnormalities</li> <li><a>Psychogenic visual loss</a></li> </ul>

109
Q

Visual Pathway Disorder. How do you manage it?

A

<ul> <li>Refer to ophthalmologist or neuro-ophthalmologist with urgency that matches speed of onset of visual loss</li> </ul>

110
Q

Visual Pathway Disorder. What will happen?

A

<ul> <li>Some disorders are reversible, especially if detected early</li> </ul>

111
Q

Vitreous Detachment. What is it?

A

<ul> <li><a>Separation of posterior vitreous</a> from its normal attachments to retina</li> <li>Brought on by aging (usually past age 60), eye trauma (including eye surgery), eye inflammation, myopia </li> <li>Often announced by new flashes and floaters </li> <li>Chief concern is <a>retinal break</a> leading to <a>retinal detachment</a></li> </ul>

112
Q

Vitreous Detachment. How does it appear?

A

<ul><li>Patient may report new <a>flashes</a> of light in affected eye</li><li>Patient may report new floater </li> <li>Ophthalmoscopy may show wispy gray fragment or ring ("<a>Weiss ring</a>"), which is... </li> <li>Condensed back surface of detached vitreous that has <a>pulled away from retinal surface</a></li><li>Detaching vitreous may <a>tear hole in retina and sometimes cause retinal detachment</a> visible on indirect ophthalmoscopy </li> </ul>

113
Q

Vitreous Detachment. What else looks like it?

A

<ul> <li>New flashes may be caused by vitreous tug on retina without vitreous detachment </li> <li>New flashes may also be caused by lesions anywhere in visual pathway </li> <li>New <a>floaters</a> can be caused by retinal bleeding into vitreous </li> <li>New floaters can also be caused by vitreous inflammation </li> </ul>

114
Q

Vitreous Detachment. How do you manage it?

A

<ul><li>Refer patient reporting new flashes and floaters urgently to ophthalmologist </li> <li>Refer even more urgently if patient also reports new visual field loss, as that suggests retinal detachment </li><li>If visual acuity has been unaffected, must still refer urgently because... </li> <li>Retinal detachment starts in peripheral retina and spreads toward fovea, and... </li> <li>Diagnosis of retinal detachment before spread to fovea predicts better visual outcome with surgery </li> </ul>

115
Q

Vitreous Detachment. What will happen?

A

<ul> <li>Retinal break occurs in fewer than 10% of patients with new vitreous detachment, and...</li> <li> Retinal detachment rare even when there has been retinal break, but... </li> <li>Symptoms do not allow distinction between those who have or have not had retinal detachment, which can only be verified by skilled ophthalmoscopy </li> <li>Retinal reattachment surgery more successful in restoring vision if detachment has not spread to fovea</li> </ul>

116
Q

Wet Age-Related Macular

A

<ul><li>Form of macular degeneration marked by...</li><li>Leakage of serum or blood into fovea from choroidal new blood vessels that have burrowed into retina ("choroidal neovascularization"), which causes...</li><li>Reduced visual acuity and distorted vision ("metamorphopsia") </li> <li>Accounts for up to 20% of cases of age-related macular degeneration</li> <li>Periodic intravitreous injection of inhibitors of vascular endothelial growth factor (VEGF) is effective in retarding and sometimes restoring vision loss </li><li>Other possibly effective treatments include thermal laser photocoagulation, photodynamic therapy, and supplementation with zinc and antioxidant vitamins </li></ul>

117
Q

Wet Age-Related Macular

A

<ul><li>Acute, subacute, or chronic painless vision loss, usually in one eye </li><li><a>Metamorphopsia</a></li><li>Yellow, brown, gray, red, or green <a>discoloration</a> and sometimes elevation in macular region</li><li>Leakage of serum and blood under fovea from <a>new but incompetent choroidal blood vessels</a> visible on fluorescein angiography</li></ul>

118
Q

Wet Age-Related Macular

A

<ul> <li>Retinal and choroidal degenerations, inflammations, infections, tumors, and trauma</li></ul>

119
Q

Wet Age-Related Macular

A

<ul><li>Refer non-urgently if this is incidental finding</li><li>Refer urgently if associated with new vision loss</li><li>Instruct patients to report to their ophthalmologist immediately if they notice sudden development of warped or blurred vision because these symptoms signal subfoveal bleeding</li></ul>

120
Q

Wet Age-Related Macular

A

<ul> <li>Traditional photocoagulation treatments, which modestly reduce pace of vision loss but do not restore vision, have mostly given way to...</li> <li>Periodic injections of VEGF inhbitors into vitreous cavity (yes, really!), which slow and sometimes reverse vision loss</li> <li>Stopping smoking and taking daily combination tablet of vitamin C 500mg, vitamin E 400 IU, zinc oxide 80mg, cupric oxide 2mg, and beta carotene 15mg reduce progression of vision loss </li></ul>