Other Eye Conditions Flashcards
Amblyopia. What is it?
<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>
Amblyopia. How does it appear?
<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>
Amblyopia. What else looks like it?
<ul><li>Uncorrected refractive error</li> <li>Lesion of ocular media, retina, or visual pathway</li><li>Psychogenic visual loss</li></ul>
Amblyopia. How do you manage it?
<ul><li>Refer non-urgently for diagnosis of provocative condition and treatment</li></ul>
Amblyopia. What will happen?
<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>
Basal Cell Carcinoma. What is it?
<ul><li>Most common malignant tumor of lid</li><li>Does not metastasize, but can burrow deep into orbit </li></ul>
Basal Cell Carcinoma. How does it appear?
<ul> <li>Slowly <a>enlarging lump</a> or plaque </li><li>Most often on lower lid </li></ul>
Basal Cell Carcinoma. What else looks like it?
<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>
Basal Cell Carcinoma. How do you manage it?
<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>
Basal Cell Carcinoma. What will happen?
<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>
Cataract. What is it?
<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>
Cataract. How does it appear?
<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>
Cataract. What else looks like it?
<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>
Cataract. How do you manage it?
<ul><li>Refer non-urgently</li></ul>
Cataract. What will happen?
<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>
Central Retinal Artery Occlusion. What is it?
<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>
Central Retinal Artery Occlusion. How does it appear?
<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>
Central Retinal Artery Occlusion. What else looks like it?
<ul><li>Nothing, but...</li> <li>Distinctive milky white retina with cherry red spot may not develop for first 24 hours</li> </ul>
Central Retinal Artery Occlusion. How do you manage it?
<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>
Central Retinal Artery Occlusion. What will happen?
<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>
Central Retinal Vein Occlusions. What is it?
<ul> <li>Blockage of flow in vein that drains inner retina</li> <li>Common causes: systemic hypertension, diabetes, arteriosclerosis, hypercoagulable states</li> </ul>
Central Retinal Vein Occlusions. How does it appear?
<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>
Central Retinal Vein Occlusions. What else looks like it?
<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>
Central Retinal Vein Occlusions. How do you manage it?
<ul> <li>Refer to ophthalmologist urgently</li> </ul>
Central Retinal Vein Occlusions. What will happen?
<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>
Choroidal Melanoma. What is it?
<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>
Choroidal Melanoma. How does it appear?
<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>
Choroidal Melanoma. What else looks like it?
<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>
Choroidal Melanoma. How do you manage it?
<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>
Choroidal Melanoma. What will happen?
<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>
Congenital Glaucoma. What is it?
<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>
Congenital Glaucoma. How does it appear?
<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>
Congenital Glaucoma. What else looks like it?
<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>
Congenital Glaucoma. How do you manage it?
<ul> <li>Refer urgently any baby with cloudy cornea</li> </ul>
Congenital Glaucoma. What will happen?
<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>
Dry Age-related Macular
<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>
Dry Age-related Macular
<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>
Dry Age-related Macular
<ul><li><a>Other yellow white things in retina</a></li></ul>
Dry Age-related Macular
<ul> <li>Refer non-urgently if this is incidental finding</li> <li>Refer urgently if the patient has new vision loss</li> </ul>
Dry Age-related Macular
<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>
Idiopathic Orbital Inflammation. What is it?
<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>
Idiopathic Orbital Inflammation. How does it appear?
<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>
Idiopathic Orbital Inflammation. What else looks like it?
<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>
Idiopathic Orbital Inflammation. How do you manage it?
<ul> <li>Refer patient urgently for clinical and imaging assessment</li> </ul>
Idiopathic Orbital Inflammation. What will happen?
<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>
Iris Melanoma. What is it?
<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>
Iris Melanoma. How does it appear?
<ul><li><a>Brown plaque on iris surface</a></li> <li>Pupil may be distorted</li> </ul>
Iris Melanoma. What else looks like it?
<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>