Other Eye Conditions

Question 1

Amblyopia. What is it?

Answer 1

<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>

Question 2

Amblyopia. How does it appear?

Answer 2

<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>

Question 3

Amblyopia. What else looks like it?

Answer 3

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

Question 4

Amblyopia. How do you manage it?

Answer 4

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

Question 5

Amblyopia. What will happen?

Answer 5

<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>

Question 6

Basal Cell Carcinoma. What is it?

Answer 6

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

Question 7

Basal Cell Carcinoma. How does it appear?

Answer 7

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

Question 8

Basal Cell Carcinoma. What else looks like it?

Answer 8

<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>

Question 9

Basal Cell Carcinoma. How do you manage it?

Answer 9

<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>

Question 10

Basal Cell Carcinoma. What will happen?

Answer 10

<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>

Question 11

Cataract. What is it?

Answer 11

<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>

Question 12

Cataract. How does it appear?

Answer 12

<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>

Question 13

Cataract. What else looks like it?

Answer 13

<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>

Question 14

Cataract. How do you manage it?

Answer 14

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

Question 15

Cataract. What will happen?

Answer 15

<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>

Question 16

Central Retinal Artery Occlusion. What is it?

Answer 16

<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>

Question 17

Central Retinal Artery Occlusion. How does it appear?

Answer 17

<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>

Question 18

Central Retinal Artery Occlusion. What else looks like it?

Answer 18

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

Question 19

Central Retinal Artery Occlusion. How do you manage it?

Answer 19

<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>

Question 20

Central Retinal Artery Occlusion. What will happen?

Answer 20

<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>

Question 21

Central Retinal Vein Occlusions. What is it?

Answer 21

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

Question 22

Central Retinal Vein Occlusions. How does it appear?

Answer 22

<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>

Question 23

Central Retinal Vein Occlusions. What else looks like it?

Answer 23

<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>

Question 24

Central Retinal Vein Occlusions. How do you manage it?

Answer 24

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

Question 25

Central Retinal Vein Occlusions. What will happen?

Answer 25

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

Question 26

Choroidal Melanoma. What is it?

Answer 26

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

Question 27

Choroidal Melanoma. How does it appear?

Answer 27

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

Question 28

Choroidal Melanoma. What else looks like it?

Answer 28

• Choroidal nevus
• Retinal pigment epithelial hypertrophy
• Choroidal inflammation
• Choroidal metastasis
• Retinal detachment

Question 29

Choroidal Melanoma. How do you manage it?

Answer 29

• Refer any patient with new vision loss with urgency depending on symptoms
• Refer non-urgently any patient with an incidentally-noted lesion in the retina or choroid

Question 30

Choroidal Melanoma. What will happen?

Answer 30

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

Question 31

Congenital Glaucoma. What is it?

Answer 31

• Malformed trabecular meshwork at birth causes elevated intraocular pressure, enlarged eye, cloudy cornea, tearing
• Surgery to repair meshwork or bypass it and lower intraocular pressure must be prompt to prevent permanent vision loss.

Question 32

Congenital Glaucoma. How does it appear?

Answer 32

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

Question 33

Congenital Glaucoma. What else looks like it?

Answer 33

• Congenital corneal dysplasias or systemic metabolic disorders causing cloudy corneas, but...
• They usually do not have elevated intraocular pressure, large eye, or tearing

Question 34

Congenital Glaucoma. How do you manage it?

Answer 34

• Refer urgently any baby with cloudy cornea

Question 35

Congenital Glaucoma. What will happen?

Answer 35

• Eye surgery to repair or bypass trabecular meshwork
• Visual outcome usually favorable, especially if detection is prompt!

Question 36

Dry Age-related Macular

Answer 36

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

Question 37

Dry Age-related Macular

Answer 37

• Starts with yellow-white discoloration of macular region owing to atrophy of retinal pigment epithelium
• Discrete round yellow-white patches called "retinal drusen" often visible

Question 38

Dry Age-related Macular

Answer 38

• Other yellow white things in retina

Question 39

Dry Age-related Macular

Answer 39

• Refer non-urgently if this is incidental finding
• Refer urgently if the patient has new vision loss

Question 40

Dry Age-related Macular

Answer 40

• Over time, drusen often increase (Watch this typical sequence)
• In worst cases, large areas of retinal atrophy appear and visual acuity declines
• 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
• Smokers will be advised to quit
• 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 ("metamorphopsia"), which might signal that...
• New blood vessels have grown from choroid into submacular retina ("subretinal neovascularization"), which has led to...
• Bleeding under the retina that further blurs and distorts vision (Wet age-related macular degeneration)
• 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

Question 41

Idiopathic Orbital Inflammation. What is it?

Answer 41

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

Question 42

Idiopathic Orbital Inflammation. How does it appear?

Answer 42

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

Question 43

Idiopathic Orbital Inflammation. What else looks like it?

Answer 43

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

Question 44

Idiopathic Orbital Inflammation. How do you manage it?

Answer 44

• Refer patient urgently for clinical and imaging assessment

Question 45

Idiopathic Orbital Inflammation. What will happen?

Answer 45

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

Question 46

Iris Melanoma. What is it?

Answer 46

• Brown pigmented mass on iris
• Low-grade malignancy
• Not associated with melanoma of skin or other tissues

Question 47

Iris Melanoma. How does it appear?

Answer 47

• Brown plaque on iris surface
• Pupil may be distorted

Question 48

Iris Melanoma. What else looks like it?

Answer 48

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

Question 49

Iris Melanoma. How do you manage it?

Answer 49

• Refer non-urgently if patient has new visual symptoms or thinks lesion new or growing

Question 50

Iris Melanoma. What will happen?

Answer 50

• Lesion suspicious for melanoma will be biopsied
• Metastasis very rare unless lesion extends into ciliary body

Question 51

Non-arteritic Ischemic Optic

Answer 51

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

Question 52

Non-arteritic Ischemic Optic

Answer 52

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

Question 53

Non-arteritic Ischemic Optic

Answer 53

• Arteritic ischemic optic neuropathy in giant cell arteritis, 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
• Optic neuritis, usually occurring in younger patients
• Papilledema, usually binocular with relatively preserved vision
• Neoplastic optic neuropathy, usually with previously known cancer

Question 54

Non-arteritic Ischemic Optic

Answer 54

• Refer urgently to ophthalmologist because of concern for arteritic ischemic optic neuropathy in giant cell arteritis

Question 55

Non-arteritic Ischemic Optic

Answer 55

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

Question 56

Open-Angle Glaucoma. What is it?

Answer 56

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

Question 57

Open-Angle Glaucoma. How does it appear?

Answer 57

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

Question 58

Open-Angle Glaucoma. What else looks like it?

Answer 58

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

Question 59

Open-Angle Glaucoma. How do you manage it?

Answer 59

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

Question 60

Open-Angle Glaucoma. What will happen?

Answer 60

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

Question 61

Optic Neuritis. What is it?

Answer 61

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

Question 62

Optic Neuritis. How does it appear?

Answer 62

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

Question 63

Optic Neuritis. What else looks like it?

Answer 63

• Retinopathies and other optic neuropathies
• Retrobulbar visual pathway disease
• Psychogenic visual loss

Question 64

Optic Neuritis. How do you manage it?

Answer 64

• Refer urgently any patient with acute or subacute vision loss

Question 65

Optic Neuritis. What will happen?

Answer 65

• 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...
• Spontaneous total or near total visual recovery occurs in 85%, and...
• Corticosteroid treatment does not affect final visual outcome or long term incidence of multiple sclerosis
• In optic neuritis associated with other autoimmune disorders, corticosteroid treatment may be very effective
• In optic neuritis associated with infections, treatment directed at those infections

Question 66

Psychogenic Visual Loss. What is it?

Answer 66

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

Question 67

Psychogenic Visual Loss. How does it appear?

Answer 67

• Most commonly as persistent monocular profound visual loss
• Less commonly as homonymous hemianopia, bitemporal hemianopia, monocular temporal hemianopia
• 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
• Malingerers aim for gain—compensation, relief from work or other obligations
• Somatizers aim to resolve depression, psychosocial conflicts or predicaments
• Hypochondriacs convinced they are ill
• Conversion hysterics trying to avoid deep psychic issues

Question 68

Psychogenic Visual Loss. What else looks like it?

Answer 68

• Organic visual loss, which can be difficult to exclude

Question 69

Psychogenic Visual Loss. How do you manage it?

Answer 69

• Refer to ophthalmologist who should have skills and tricks to unmask this condition

Question 70

Psychogenic Visual Loss. What will happen?

Answer 70

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

Question 71

Refractive Disorders. What is it?

Answer 71

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

Question 72

Refractive Disorders. How does it appear?

Answer 72

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

Question 73

Refractive Disorders. What else looks like it?

Answer 73

• Lesions of the ocular media, retina, and visual pathway

Question 74

Refractive Disorders. How do you manage it?

Answer 74

• Refer to vision care providers, who are able to detect and correct refractive errors and distinguish them from other causes of impaired vision

Question 75

Refractive Disorders. What will happen?

Answer 75

• Nearly all refractive errors can be corrected with spectacles or contact lenses, or by surgically reshaping cornea
• Myopia is corrected with a spherical concave lens that moves the focus backwards in the eye so that it falls onto the retina
• Hyperopia is corrected with a spherical convex lens that moves the focus forward onto the retina
• Astigmatism is corrected with a cylindrical lens, which has more focusing power in one axis than another
• 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
• Presbyopia is corrected 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

Question 76

Retinal Break. What is it?

Answer 76

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

Question 77

Retinal Break. How does it appear?

Answer 77

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

Question 78

Retinal Break. What else looks like it?

Answer 78

• Vitreous tug on retina without retinal break
• Vitreous separation from retina without retinal break

Question 79

Retinal Break. How do you manage it?

Answer 79

• Refer urgently patient with new-onset flashes or floaters

Question 80

Retinal Break. What will happen?

Answer 80

• Retinal break may need to be repaired to prevent retinal detachment

Question 81

Retinal Detachment. What is it?

Answer 81

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

Question 82

Retinal Detachment. How does it appear?

Answer 82

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

Question 83

Retinal Detachment. What else looks like it?

Answer 83

• Retinal break
• Vitreous detachment
• Other retinopathies

Question 84

Retinal Detachment. How do you manage it?

Answer 84

• Refer urgently any patient with symptoms suggesting retinal detachment

Question 85

Retinal Detachment. What will happen?

Answer 85

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

Question 86

Retinoblastoma. What is it?

Answer 86

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

Question 87

Retinoblastoma. How does it appear?

Answer 87

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

Question 88

Retinoblastoma. What else looks like it?

Answer 88

• Leukocoria also caused by many other vitreoretinal disorders, usually separable from retinoblastoma by ophthalmoscopy, ultrasound, optical coherence tomography, CT, MRI

Question 89

Retinoblastoma. How do you manage it?

Answer 89

• Check for leukocoria and strabismus in babies and screen for subnormal vision in young children
• Refer suspicious cases within weeks

Question 90

Retinoblastoma. What will happen?

Answer 90

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

Question 91

Retinopathy of Prematurity. What is it?

Answer 91

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

Question 92

Retinopathy of Prematurity. How does it appear?

Answer 92

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

Question 93

Retinopathy of Prematurity. What else looks like it?

Answer 93

• Nothing, but...
• Challenge is to recognize subtle early signs so that...
• Baby can be examined frequently to detect dangerous progression

Question 94

Retinopathy of Prematurity. How do you manage it?

Answer 94

• Arrange for at-risk babies to be examined at about 4 weeks after birth by ophthalmologist skilled in screening for this condition

Question 95

Retinopathy of Prematurity. What will happen?

Answer 95

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

Question 96

Strabismus. What is it?

Answer 96

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

Question 97

Strabismus. How does it appear?

Answer 97

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

Question 98

Strabismus. What else looks like it?

Answer 98

• Wide nasal bridge gives false impression of convergent strabismus ("pseudostrabismus")
• Displacement of an eye by orbital tumor or trauma may give false impression of misalignment
• Ptosis or lid retraction may give false impression of misalignment

Question 99

Strabismus. How do you manage it?

Answer 99

• Confirm strabismus by performing cover test and eliciting fixational eye movement, or...
• Noting if diplopia disappears as patient covers either eye
• 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...
• If you are not sure of your test results or patient reports diplopia...
• Refer with urgency that depends on how recently strabismus was noted and on accompanying pertinent findings, because...
• Brain aneurysm or other life-threatening conditions could be present

Question 100

Strabismus. What will happen?

Answer 100

• Strabismus in early childhood often accompanied by amblyopia, which must be promptly treated to prevent persistent vision loss
• Treatment of strabismus depends on underlying cause
• 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")
• Causes in adults are internuclear ophthalmoplegia, skew deviation, cranial nerve palsies, myasthenia gravis, extraocular muscle inflammation, and orbital trauma
• Most urgent diagnosis is third cranial nerve palsy because could be caused by brain aneurysm with imminent rupture and death

Question 101

Tonic Pupil. What is it?

Answer 101

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

Question 102

Tonic Pupil. How does it appear?

Answer 102

• 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
• Slit lamp examination often shows that pupil constricts segmentally (stromal streaming)
• Accommodation may be impaired in affected eye
• Deep tendon reflexes may be absent

Question 103

Tonic Pupil. What else looks like it?

Answer 103

• Iris damage from trauma, intraocular surgery, inflammation
• Accidental or deliberate ocular instillation of anticholinergic substances

Question 104

Tonic Pupil. How do you manage it?

Answer 104

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

Question 105

Tonic Pupil. What will happen?

Answer 105

• Life-long condition but does not cause troublesome symptoms
• Affected pupil often becomes smaller than unaffected pupil
• No related medical problems will emerge, but...
• Pupil of other eye may later become similarly affected
• 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

Question 106

Visual Pathway Disorder. What is it?

Answer 106

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

Question 107

Visual Pathway Disorder. How does it appear?

Answer 107

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

Question 108

Visual Pathway Disorder. What else looks like it?

Answer 108

• Undetected refractive error
• Subtle ocular media abnormalities
• Subtle retinal abnormalities
• Psychogenic visual loss

Question 109

Visual Pathway Disorder. How do you manage it?

Answer 109

• Refer to ophthalmologist or neuro-ophthalmologist with urgency that matches speed of onset of visual loss

Question 110

Visual Pathway Disorder. What will happen?

Answer 110

• Some disorders are reversible, especially if detected early

Question 111

Vitreous Detachment. What is it?

Answer 111

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

Question 112

Vitreous Detachment. How does it appear?

Answer 112

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

Question 113

Vitreous Detachment. What else looks like it?

Answer 113

• New flashes may be caused by vitreous tug on retina without vitreous detachment
• New flashes may also be caused by lesions anywhere in visual pathway
• New floaters can be caused by retinal bleeding into vitreous
• New floaters can also be caused by vitreous inflammation

Question 114

Vitreous Detachment. How do you manage it?

Answer 114

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

Question 115

Vitreous Detachment. What will happen?

Answer 115

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

Question 116

Wet Age-Related Macular

Answer 116

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

Question 117

Wet Age-Related Macular

Answer 117

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

Question 118

Wet Age-Related Macular

Answer 118

• Retinal and choroidal degenerations, inflammations, infections, tumors, and trauma

Question 119

Wet Age-Related Macular

Answer 119

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

Question 120

Wet Age-Related Macular

Answer 120

• Traditional photocoagulation treatments, which modestly reduce pace of vision loss but do not restore vision, have mostly given way to...
• Periodic injections of VEGF inhbitors into vitreous cavity (yes, really!), which slow and sometimes reverse vision loss
• 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