Opthalmoscopic Abnormalities Flashcards
Arteriovenous Nicking. What is it?
<ul> <li>Indentation (nicking) of retinal veins by stiff (arteriosclerotic) retinal arteries </li> <li>Commonest cause is chronic hypertension</li> <li>Valuable sign of chronic systemic hypertension that has also caused damage to arteries elsewhere in body (heart, kidneys, brain) </li> </ul>
Arteriovenous Nicking. How does it appear?
<ul> <li>At <a>arteriovenous crossing points</a>, retinal vein is deviated and narrowed by overlying retinal artery </li> </ul>
Arteriovenous Nicking. What else looks like it?
<ul> <li>Nothing</li> </ul>
Arteriovenous Nicking. How do you manage it?
<ul><li>Using ophthalmoscope, find these vessels at their emergence from optic disc and follow them as far out as you can, looking for arteriovenous nicking, which is usually found within 5 disc diameters of optic disc </li> <li>Measure blood pressure and inquire after other arteriosclerotic risk factors</li> </ul>
Arteriovenous Nicking. What will happen?
<ul> <li>Uncontrolled systemic blood pressure has severe health consequences</li> </ul>
Branch Retinal Artery Occlusion . What is it?
<ul> <li>Ischemic swelling of portion of retina served by occluded branch of retinal artery</li> <li>In this case, occlusion occurred because of embolus, visible as <a>yellow-white particle</a> at vessel bifurcation</li> <li>Patient reported sudden painless cloudy vision in upper field of vision of left eye</li> </ul>
Branch Retinal Artery Occlusion . How does it appear?
<ul> <li>History of sudden painless loss of upper field leads you there</li> <li>Ischemic retina has lost its transparency, now appearing gray instead of transmitting orange color of underlying choroid</li> </ul>
Branch Retinal Artery Occlusion . What else looks like it?
<ul> <li><a>Inflammatory retinal infiltrate</a>, BUT...would have fuzzier edges</li><li><a>Choroidal tumor</a>, BUT...would be more subtle color change</li> <li><a>Retinal detachment</a>, BUT...would be more extensive</li> </ul>
Branch Retinal Artery Occlusion . How do you manage it?
<ul> <li>Interpret this finding as indication of embolism from cervical carotid artery or heart</li> <li>Refer to ophthalmologist urgently if vision loss came on recently</li> </ul>
Branch Retinal Artery Occlusion . What will happen?
<ul> <li>Further embolization causing stroke could be imminent and potentially prevented with urgent medical attention</li> </ul>
Congenitally Elevated Optic Disc Anomaly. What is it?
<ul> <li>Optic disc elevation present from birth</li> <li>Probably caused by small scleral opening so that optic nerve axons are tight fit</li> <li>Other dysplastic features may contribute to elevation</li> <li>Usually does not disturb vision</li> </ul>
Congenitally Elevated Optic Disc Anomaly. How does it appear?
<ul> <li>There is no physiologic cup; compare to <a>normal physiologic cup</a></li> <li>Nerve fiber layer adjacent to optic disc not obscured as it would be in acquired causes of optic disc elevation ("<a>papilledema</a>")</li> <li>No <a>optic disc surface hemorrhages</a> or <a>cotton wool spots</a></li> <li>Dome-shaped rather than <a>doughnut-shaped optic disc elevation</a>, characteristic of papilledema</li> <li><a>Optic disc drusen</a>-glistening white chunks sometimes appear on optic disc surface; they are calcified mitochondria extruding from axons</li></ul>
Congenitally Elevated Optic Disc Anomaly. What else looks like it?
<ul> <li><a>Papilledema</a></li> <li>Other causes of acquired optic disc elevation</li> </ul>
Congenitally Elevated Optic Disc Anomaly. How do you manage it?
<ul> <li>Refer to ophthalmologist non-urgently if this is isolated finding in asymptomatic patient</li> <li>Refer urgently if patient has symptoms to suggest vision loss or increased intracranial pressure</li> </ul>
Congenitally Elevated Optic Disc Anomaly. What will happen?
<ul> <li>Even experienced eye care providers cannot always distinguish congenitally elevated optic disc anomaly from acquired optic disc elevation by ophthalmoscopy alone, therefore...</li> <li>Non-ophthalmoscopic clues must be used to make this distinction</li> <li>Examiners will mistake congenitally elevated optic disc elevation for papilledema over and over</li> <li>Congenitally elevated optic disc elevation with drusen may be associated with visual field loss that may be progressive</li></ul>
Copper-Wiring and Silver-Wiring. What is it?
<ul><li>Thickening of walls of retinal arterioles from chronic hypertension</li> </ul>
Copper-Wiring and Silver-Wiring. How does it appear?
<ul> <li>Retinal arterioles appear orange or yellow instead of red ("<a>copper wiring</a>")</li> <li>Retinal arterioles look white if they have become occluded ("<a>silver wiring</a>")</li> <li>Retinal arterioles indent retinal veins as they cross each other ("<a>arteriovenous nicking</a>")</li> </ul>
Copper-Wiring and Silver-Wiring. What else looks like it?
<ul> <li>Nothing—your challenge is to recognize this sign! </li> </ul>
Copper-Wiring and Silver-Wiring. How do you manage it?
<ul><li>Recognize these signs of chronically elevated blood pressure</li> <li>Measure blood pressure, but even if not currently elevated, assume it has been elevated in past</li> <li>Make sure blood pressure is controlled </li> </ul>
Copper-Wiring and Silver-Wiring. What will happen?
<ul> <li>Poor blood pressure control has adverse consequences—heart attack, stroke, and kidney disease among them</li> </ul>
Cotton Wool Spots. What is it?
<ul> <li>White spots on retinal surface caused by microinfarction</li> <li>Usually do not produce vision loss unless large or near fovea </li> <li>Causes are hypertension, diabetes, HIV, lupus, severe anemia or thrombocytopenia, hypercoagulable states, connective tissue disorders, viruses, lues, Behçet, Purtscher, and many others</li> </ul>
Cotton Wool Spots. How does it appear?
<ul> <li>Like dabs of white paint within 5 optic disc diameters of optic disc</li> </ul>
Cotton Wool Spots. What else looks like it?
<ul> <li>Retinal drusen, chorioretinal atrophy, inflammatory retinal infiltrate, myelinated nerve fibers</li> <li>These <a>yellow-white things in retina</a> are difficult to distinguish from each other</li> </ul>
Cotton Wool Spots. How do you manage it?
<ul> <li>Refer to ophthalmologist non-urgently if incidental finding, urgently if associated with active illness or new vision loss</li> </ul>
Cotton Wool Spots. What will happen?
<ul> <li>Depends on underlying cause</li> </ul>
Myelinated Nerve Fibers. What is it?
<ul> <li>White patches on retinal surface that often surround optic disc </li> <li>May cover large area, as in this picture</li> <li>Congenital anomaly in which retinal nerve fibers are mistakenly myelinated </li> <li>Does not interfere with vision </li> </ul>
Myelinated Nerve Fibers. How does it appear?
<ul><li>Like <a>white paint</a> spread over retinal surface that obscures vessels </li> </ul>
Myelinated Nerve Fibers. What else looks like it?
<ul> <li><a>Cotton wool spots</a>, BUT...myelinated nerve fibers are larger and denser and almost always connected to optic disc</li> <li><a>Retinal infiltrates</a>, BUT...they often have overlying vitreous haze</li> <li><a>Papilledema</a>, BUT... myelinated nerve fibers are much whiter and extend farther out on retina </li> <li><a>Hard exudates</a>, BUT...they are smaller and yellower and located farther from optic disc</li><li>Check out <a>yellow-white things in the retina</a></li></ul>
Myelinated Nerve Fibers. How do you manage it?
<ul> <li>If you are confident of diagnosis, reassure patient </li> <li>If not, refer to ophthalmologist non-urgently if no new symptoms </li> </ul>
Myelinated Nerve Fibers. What will happen?
<ul> <li>Stable condition that does not affect vision</li> <li>Important mainly because it alarms examiners</li> </ul>
Old Retinal Vascular Occlusion. What is it?
<ul> <li>White, thready retinal vessels that look like twisted pipe cleaners </li> <li>There is no retinal edema to indicate recent infarction because these vessels were occluded long ago</li> <li>Many conditions cause this, including hypertension, connective tissue disease, Behçet disease, sarcoidosis</li> <li>Patient has patchy scotomas in visual field corresponding to infarcted retina<br></br> </li> </ul>
Old Retinal Vascular Occlusion. How does it appear?
<ul><li><a>White segments</a> interrupt red blood column in retinal vessels</li> </ul>
Old Retinal Vascular Occlusion. What else looks like it?
<ul> <li>Nothing</li> </ul>
Old Retinal Vascular Occlusion. How do you manage it?
<ul> <li>Interpret this as sign of old vascular occlusion </li> <li>Blood vessels in other body tissues are probably similarly affected but you cannot see them </li> </ul>
Old Retinal Vascular Occlusion. What will happen?
<ul> <li>This finding may be clue to systemic vasculopathy which, if active, will go on to destroy tissue elsewhere in body</li> </ul>
Optic Disc Pallor. What is it?
<ul> <li>Whiteness of optic disc neuroretinal rim on ophthalmoscopy</li> <li>Sign of death of optic nerve axons</li> <li>Appears weeks to months after axons have died</li> <li>Many diseases can cause this</li> </ul>
Optic Disc Pallor. How does it appear?
<ul> <li>In normal eyes, <a>physiologic cup</a> in center of optic disc appears white, but <a>neuroretinal rim</a> appears orange on ophthalmoscopy</li> <li>In optic disc pallor, neuroretinal rim appears <a>white instead of orange</a></li> <li>Color change may be subtle</li> </ul>
Optic Disc Pallor. What else looks like it?
<ul> <li><a>Normal optic disc</a>, whose temporal portion is whiter than its nasal portion</li> <li><a>Optic disc of myopic patients</a>, whose temporal portion is even whiter than in non-myopic patients</li> <li>Distinguishing pathologic optic pallor from normal variation and myopic optic discs is very challenging and best left to ophthalmologist</li> </ul>
Optic Disc Pallor. How do you manage it?
<ul> <li>If you suspect optic disc pallor, refer non-urgently to ophthalmologist</li> </ul>
Optic Disc Pallor. What will happen?
<ul> <li>Optic disc pallor means that optic nerve axons have been damaged in variety of disorders</li> <li>Delayed diagnosis may lead to irreversible blindness</li> </ul>
Papilledema. What is it?
<ul> <li>Swelling of optic disc caused by increased intracranial pressure </li> </ul>
Papilledema. How does it appear?
<ul> <li>Patient may report transient black-outs of vision, especially upon standing </li> <li>Patient need not report headache or other non-visual symptoms </li> <li>Optic disc margins <a>indistinct</a></li> <li>Optic disc elevated above retinal surface </li> <li>These signs may be ophthalmoscopically subtle </li> <li>In acute phase, may see <a>hemorrhages</a> and <a>cotton wool spots </a></li> <li>In <a>chronic phase</a>, optic disc elevation and blurred margins, but no hemorrhages or cotton wool spots</li> <li> In <a>atrophic phase</a> (optic nerve axons have died), optic disc shows mixture of pallor and swelling</li> <li>Vision usually normal or near normal unless atrophy has set in </li> </ul>
Papilledema. What else looks like it?
<ul> <li><a>Congenitally elevated optic disc</a>, but features of dysplasia usually present and visual function usually preserved</li> <li><a>Non-arteritic ischemic optic neuropathy</a>, but patient reports acute unilateral vision loss, and optic disc swelling usually unilateral</li> <li>Arteritic ischemic optic neuropathy in <a>giant cell arteritis</a>, but patient usually has systemic symptoms </li> <li>Optic neuritis, but patient reports acute vision loss and sometimes periocular pain in affected eye on gaze from side to side</li> <li>Compressive optic neuropathy from mass in orbit or optic canal, but lesion visible on imaging </li> <li>Infiltrative optic neuropathy from metastatic cancer or systemic inflammation like sarcoidosis, but there is usually evidence of cancer or inflammation elsewhere </li> <li>Leber hereditary optic neuropathy, but usually unilateral and optic disc is hyperemic</li><li><a>Central retinal vein occlusion</a>, but that has more hemorrhage and less optic disc swelling</li><li><a>Terson syndrome</a>, but only in setting of severe body trauma or pancreatitis</li> <li>Distinguishing these causes of optic disc edema is challenging</li></ul>
Papilledema. How do you manage it?
<ul> <li>Refer emergently (within 24 hours) to ophthalmologist if you detect elevated optic discs and patient has visual, neurologic, or constitutional symptoms </li> <li>Refer urgently (within 48 hours) if you detect elevated optic discs in an asymptomatic patient </li> </ul>
Papilledema. What will happen?
<ul> <li>Ophthalmologist will try to determine cause of elevated optic disc </li> <li>If papilledema is suspected, patient will undergo immediate neurologic examination and brain imaging </li> <li>If arteritic ischemic optic neuropathy is suspected, patient will undergo prompt intensive corticosteroid treatment and temporal artery biopsy</li> <li>If compressive optic neuropathy is suspected, patient will undergo orbit and brain imaging </li> <li>If infiltrative optic neuropathy is suspected, patient will undergo orbit/brain imaging, lumbar puncture, and search for evidence of metastatic cancer or systemic inflammation </li> <li>If Leber optic neuropathy is suspected, patient will undergo blood testing for appropriate mitochondrial gene mutations </li> <li>Undiagnosed chronic papilledema may lead to death of optic nerve axons and dreadful and irreversible vision loss, therefore... </li> <li>Early detection of papilledema is critical, not only to discover and treat its cause, but to relieve pressure on optic nerves </li> </ul>
Pathologic Optic Disc Cupping. What is it?
<ul><li><a>Thinning of optic disc neuroretinal rim</a> so that optic disc appears pathologically cupped (excavated)</li> <li>Usual cause is <a>glaucoma</a></li> <li>Glaucoma causes slow death of optic nerve axons and their supporting glia partly because of chronically high intraocular pressure</li> <li>Visual fields eventually become constricted, but only when neuroretinal rim is very thinned</li> <li>Intraocular pressure must be controlled to forestall worsening of vision </li> </ul>
Pathologic Optic Disc Cupping. How does it appear?
<ul> <li>Enlarged cup to disc ratio (optic disc cup diameter greater than ½ of optic disc diameter)</li></ul>
Pathologic Optic Disc Cupping. What else looks like it?
<ul> <li>Physiologically large optic disc cups, BUT...neuroretinal rim is not thinned and cup is not vertically elongated</li> <li><a>Coloboma of optic disc</a>, BUT...this is congenital abnormality</li> <li><a>Tilted disc of myopia</a>, BUT...features of tilting give this away</li> <li>Non-glaucomatous optic neuropathy, BUT...there will be non-ophthalmoscopic clues to this diagnosis</li> <li>Distinguishing pathologic optic disc cupping from physiologically large cups, coloboma, and myopic tilt may be difficult by ophthalmoscopy alone </li> </ul>
Pathologic Optic Disc Cupping. How do you manage it?
<ul> <li>Identify pathologic optic disc cupping by ophthalmoscopy</li> <li>Do not try to distinguish between one cause and another</li> <li>Refer to ophthalmologist non-urgently </li> </ul>
Pathologic Optic Disc Cupping. What will happen?
<ul> <li>Undetected glaucoma can progress to marked and irreversible vision loss </li> <li>Control of intraocular pressure is often effective at arresting or slowing down progression of glaucoma</li> </ul>
Purtscher Retinopathy. What is it?
<ul> <li>Multiple microinfarctions of retina</li> <li>Evident as cotton wool spots, usually in both eyes</li> <li>Presumed antigen-antibody clumping in arterioles with complement release</li> <li>Usually only evidence of infarction</li> <li>Occurs immediately in severe compressive chest, pelvic, long bone trauma, pancreatitis</li> <li>Patient usually reports scotomas</li> </ul>
Purtscher Retinopathy. How does it appear?
<ul> <li>Scotomatous visual loss in one eye or both</li> <li>May impair visual acuity </li> <li>Multiple <a>cotton wool spots</a> within temporal vascular arcades of retina</li> <li>Scattered retinal hemorrhages sometimes</li> <li>Patient (and caregivers) usually preoccupied with non-ophthalmic manifestations</li> </ul>
Purtscher Retinopathy. What else looks like it?
<ul><li>Acute <a>systemic hypertension</a></li> <li><a>Diabetes mellitus</a>, but should have more small retinal hemorrhages</li> <li><a>Embolic retinopathy</a>, but should have intraretinal plaques</li> <li><a>Connective tissue diseases</a></li> <li><a>Vasculitis</a>, but should have vascular sheathing </li> </ul>
Purtscher Retinopathy. How do you manage it?
<ul> <li>Refer patient promptly with acute visual complaints in setting of trauma, pancreatitis</li> </ul>
Purtscher Retinopathy. What will happen?
<ul> <li>No treatment for this condition, but...</li> <li>Referral appropriate to confirm diagnosis </li> <li>Cotton wool spots disappear within weeks, but there may be permanent visual loss</li> </ul>
Retinal Calcific Embolus. What is it?
<ul><li>Calcium fleck embedded in retinal artery that traveled from calcified aortic valve </li> <li>May obstruct blood flow to retina, causing transient—or even persistent—visual loss in eye</li> <li>Other calcific emboli may later plug arteries in brain to cause stroke </li> </ul>
Retinal Calcific Embolus. How does it appear?
<ul> <li><a>White fleck</a> lying in artery and interrupting red blood column </li> <li>May cause infarction ("ischemic retinal whitening") of retina beyond blockage point (<a>branch retinal artery occlusion</a>)</li> <li>Patient may report vision loss </li> </ul>
Retinal Calcific Embolus. What else looks like it?
<ul><li><a>Platelet-fibrin (Hollenhorst) plaque</a> that has traveled from arteriosclerotic plaque in cervical carotid bifurcation, BUT... </li> <li>Calcium plaque is whiter than Hollenhorst plaque and usually gets stuck at more proximal retinal arteriolar branch point </li> </ul>
Retinal Calcific Embolus. How do you manage it?
<ul> <li>Interpret this as sign of abnormal aortic valve and refer for cardiac evaluation </li> </ul>
Retinal Calcific Embolus. What will happen?
<ul> <li>If source not eliminated, future emboli may travel to other parts of brain and cause stroke or further vision loss</li> </ul>
Retinal Drusen. What is it?
<ul> <li>Yellow-white flecks (retinal drusen) scattered around macular region; these are "tombstones" of dead retinal pigment epithelium </li> <li>Cause is often age-related macular degeneration, poorly understood disorder of aging </li> <li><a>Dry form of age-related macular degeneration</a> makes up 90% of cases, consisting of drusen and atrophic pigment epithelium </li> <li><a>Wet form of age-related macular degeneration</a> makes up 10% of cases, consisting of choroidal vessels burrowing into retina to cause bleeding</li></ul>
Retinal Drusen. How does it appear?
<ul> <li>Dry form displays <a>yellow-white flecks</a> and sometimes chorioretinal atrophy </li> <li>Wet form displays reddish-blue mound at fovea made up of <a>deep hemorrhage</a> and scarring</li> </ul>
Retinal Drusen. What else looks like it?
<ul> <li>Drusen of dry form can be mistaken for other <a>yellow-white things in retina</a></li> <li>Wet form can look like retinal tumor or <a>infiltrate</a></li> </ul>
Retinal Drusen. How do you manage it?
<ul> <li>If vision loss has been mild or only slowly progressive, refer to ophthalmologist non-urgently </li> <li>If vision loss has been severe or acute, refer to ophthalmologist urgently</li> </ul>
Retinal Drusen. What will happen?
<ul> <li>Dry form causes slowly progressive visual acuity loss </li> <li>National Eye Institute (NEI) study found that patients with "moderate" or "severe" disease (large, confluent drusen) could have progression slowed by taking vitamin C and E, zinc, and copper available in commercial formulations </li> <li>NEI study also found smoking adversely affects progression </li> <li>NEI study underway to test other anti-oxidants </li> <li>Wet form causes sudden and often devastating vision loss </li> <li>Periodic anti-vascular endothelial growth factor (VEGF) intravitreal injections have been dramatically successful in reducing progression of wet form, especially if caught early </li> </ul>
Retinal Hard Exudates. What is it?
<ul> <li>Yellow flecks made up of lipid residues of serous leakage from damaged capillaries</li> <li>Diabetes main cause, but also neuroretinitis, retinal vein occlusion,Von Hippel-Lindau Disease, other vascular dysplasias, radiation-induced retinal vasculopathy </li> </ul>
Retinal Hard Exudates. How does it appear?
<ul> <li><a>Yellow flecks</a> mostly between temporal vascular arcades, sometimes in distinctive circular pattern as if vessel leak were in center</li> </ul>
Retinal Hard Exudates. What else looks like it?
<ul> <li>Many other <a>yellow-white things in retina</a></li></ul>
Retinal Hard Exudates. How do you manage it?
<ul> <li>Refer to ophthalmologist non-urgently if patient has no new symptoms, and urgently if patient has new symptoms</li> </ul>
Retinal Hard Exudates. What will happen?
<ul> <li>Hard exudates are indication of excessive retinal vascular permeability caused by many vision-threatening and even life-threatening disorders</li> </ul>
Retinal Hemorrhages. What is it?
<ul><li>Hemorrhages in retina at various levels</li></ul>
Retinal Hemorrhages. How does it appear?
<ul> <li>May be present near optic disc or only in retinal periphery (<a>sickle cell retinopathy</a>)</li> <li><a>Dot/blot hemorrhages</a> <ul><li>Rupture of deep capillaries submerged within retina and caused by arteriolar, capillary, or venular incompetence</li> <li>Commonly associated with diabetes</li></ul> </li> <li><a>Flame hemorrhages</a><ul><li>Rupture on retinal nerve fiber layer of superficial pre-capillary arterioles, small veins </li> <li>Commonly associated with systemic hypertension, leukemia, severe anemia, thrombocytopenia, retinal vein occlusion, trauma</li></ul></li><li><a>Boat-shaped (pre-retinal) hemorrhages</a> <ul><li>Rupture of large superficial retinal veins into space between retina and vitreous; sometimes these bleeds break into vitreous cavity</li><li>Meniscus looks like rudder of boat </li> <li>Commonly associated with sudden increase in intracranial pressure, anemia, thrombocytopenia, trauma, vigorous headshaking in abused infants, retinal vein occlusion </li> </ul></li><li><a>Subretinal hemorrhages</a> <ul><li>Rupture of choroidal vessels under fovea in interface between choroid and retina</li> <li>Commonly associated with age-related macular degeneration</li></ul></li> <li><a>Vitreous hemorrhages</a> <ul><li>Rupture of superficial retinal vessels or vessels on fibrovascular stalk extending into vitreous</li> <li>Commonly associated with proliferative diabetic retinopathy, hypertension, trauma</li></ul></li></ul>
Retinal Hemorrhages. What else looks like it?
<ul><li>Not much; black pigment can resemble hemorrhage</li> </ul>
Retinal Hemorrhages. How do you manage it?
<ul><li>Most retinal hemorrhages can be spotted near optic disc, but there are many conditions where they are present only in retinal periphery, requiring viewing with special instruments</li> </ul>
Retinal Hemorrhages. What will happen?
<ul><li>Retinal hemorrhages are critical indicators of diseases with vascular incompetence</li><li>May be only sign of abusive head trauma, blood dyscrasia, diabetes, hypertension, sickle cell disease, lupus erythematosus, and other systemic diseases </li> </ul>
Retinal Infiltrate. What is it?
<ul> <li>Local inflammation of retina</li><li>Consists of inflammatory cells, dead retinal tissue, and perhaps micro-organisms</li> <li>Causes are infection with toxoplasmosis, herpes viruses, fungi, or bacteria, or non-infectious inflammation by sarcoidosis and other autoimmune disorders</li> </ul>
Retinal Infiltrate. How does it appear?
<ul><li><a>Fuzzy-edged yellow-white area</a> that covers part of retina </li><li>Indistinct margins and overlying vitreous haze</li></ul>
Retinal Infiltrate. What else looks like it?
<ul><li><a>Retinal ischemia</a>, BUT... infiltrates conform to vascular territory</li> <li><a>Retinal detachment</a>, BUT...detachments are more extensive</li> <li>Other <a>yellow-white things in retina</a></li></ul>
Retinal Infiltrate. How do you manage it?
<ul> <li>Interpret this as sign of infection or autoimmune reaction and refer urgently to ophthalmologist</li> </ul>
Retinal Infiltrate. What will happen?
<ul> <li>Some retinal infections, like those caused by herpes viruses, spread quickly to destroy retina unless treated vigorously</li> </ul>
Retinal Neovascularization. What is it?
<ul> <li>Tangle of new blood vessels on retinal surface </li> <li>Crude attempt at vascularizing ischemic retina</li> <li>Commonest cause is diabetes, also sickle cell disease, retinopathy of prematurity, retinal vein occlusion, severe carotid stenosis</li> <li>New vessels ("neovascularization") grow in response to vascular endothelial growth factor (VEGF) liberated by hypoxic retina</li> <li>Lacking integrity and bifurcating pattern of <a>normal vessels</a>, these new vessels bleed spontaneously or with minimal trauma </li> <li>Retinal and vitreous hemorrhages attract fibroglial elements that form <a>fibrovascular stalks</a></li> <li>These stalks induce vitreous contraction that tugs on retina until it bleeds and detaches</li> </ul>
Retinal Neovascularization. How does it appear?
<ul> <li><a>New blood vessels form net of small curls</a> in places where no blood vessels belong </li> <li>Divided into those that appear on optic disc surface (“new vessels on discâ€) and on retina (“new vessels elsewhereâ€), mostly within view of direct ophthalmoscope</li> </ul>
Retinal Neovascularization. What else looks like it?
<ul> <li>Collateral vessels that become dilated to bypass occluded vessel, BUT...they are not as curly or as profuse</li> </ul>
Retinal Neovascularization. How do you manage it?
<ul> <li>Interpret this finding as indication of severely ischemic retina</li> <li>Refer non-urgently to ophthalmologist</li> </ul>
Retinal Neovascularization. What will happen?
<ul> <li>These abnormal vessels are apt to bleed without much provocation and cause immense harm to sight</li> <li>Intravitreal injections of anti-vascular endothelial growth vactor (VEGF) agents are effective, as is retinal photocoagulation</li> <li>If diabetes is cause, strict blood sugar control is imperative</li> <li>If poor carotid artery flow is cause, endarterectomy or stenting of that vessel may be helpful </li> </ul>
Retinal Pigment Epitheliopathy. What is it?
<ul> <li>Destruction of retinal pigment epithelium, migration of black pigment, extreme narrowing of retinal vessels, optic disc pallor</li> <li>Usually caused by hereditary disorders ("retinitis pigmentosa"), rarely by paraneoplastic or other autoimmune disorders, intra-uterine inflammatory, and acquired toxic-metabolic-neurodegenerative disorders</li> <li>Two retinal areas are most vulnerable: mid-peripheral (equatorial) and perifoveal regions</li> <li>Patient usually has constricted visual field and poor night vision ("nyctalopia") </li> <li>Eventually foveal region itself becomes damaged and visual acuity fails </li> </ul>
Retinal Pigment Epitheliopathy. How does it appear?
<ul> <li>Often with family history of retinal degeneration, night vision difficulty, progressive neurologic illness, unusual medication use</li><li>Look for <a>narrowed retinal vessels</a> and black pigment</li> <li>Black pigment that may be <a>clumpy ("bone spicular")</a>, as in hereditary degenerations, or <a>very fine</a>, as in intra-uterine inflammations like rubella</li> </ul>
Retinal Pigment Epitheliopathy. What else looks like it?
<ul> <li>Old retinal artery occlusion, BUT...usually in one eye only </li> <li>Ocular trauma, BUT...usually in one eye only </li> <li>Old retinal detachment, BUT...history of repair </li> <li>Posterior uveitis, BUT...retinal vessels not so narrowed and less pigment migration </li> </ul>
Retinal Pigment Epitheliopathy. How do you manage it?
<ul> <li>Refer to ophthalmologist non-urgently unless vision loss is rapidly progressing </li> </ul>
Retinal Pigment Epitheliopathy. What will happen?
<ul> <li>Genetically-determined retinopathies typically progress slowly </li> <li>There is no treatment, but genetic counseling is important </li> <li>Paraneoplastic retinopathy may progress faster, and there is controversy as to whether discovering underlying tumor or instituting immune-modulating treatment helps slow down visual loss, BUT earlier detection of tumor may improve survival</li> <li>Autoimmune retinopathy may exist in isolation, but there is controversy about whether it is true entity and whether any form of treatment helps </li> </ul>
Retinal Platelet-fibrin (Hollenhorst) Embolus. What is it?
<ul> <li>Platelet-fibrin particle traveling from atheromatous cervical carotid bifurcation</li> <li>Named after Robert Hollenhorst, MD, who noted its connection to diseased carotid artery </li> <li>Usually causes transient vision loss as it first obstructs flow and then moves on distally </li> <li>May cause persistent vision loss from <a>segmental retinal infarct</a> </li> </ul>
Retinal Platelet-fibrin (Hollenhorst) Embolus. How does it appear?
<ul> <li><a>Yellow-white fleck</a> trapped at bifurcation of retinal arterioles </li></ul>
Retinal Platelet-fibrin (Hollenhorst) Embolus. What else looks like it?
<ul> <li><a>Retinal calcific embolus</a>, BUT...that is whiter and larger and usually trapped in straight segment of retinal artery</li> </ul>
Retinal Platelet-fibrin (Hollenhorst) Embolus. How do you manage it?
<ul> <li>Interpret this as sign of atheromatous cervical carotid disease </li> <li>Refer urgently to ophthalmologist for confirmation or to internist for vascular imaging</li> </ul>
Retinal Platelet-fibrin (Hollenhorst) Embolus. What will happen?
<ul> <li>Warning sign of unstable cervical carotid atheroma with potential for future stroke </li> <li>Greatest threat of future stroke is within days of ophthalmic event</li> </ul>
Retinal Vasculitis. What is it?
<ul><li>White cuff around retinal vessels that looks like frosting ("vascular sheathing")</li> <li>Made up of perivascular lymphocytes</li> <li>Caused by vascular inflammation ("vasculitis") associated with sarcoidosis, Behçet disease, and other autoimmune conditions</li> </ul>
Retinal Vasculitis. How does it appear?
<ul><li>Retinal vessel (usually vein) segmentally surrounded by <a>thin white cuff</a> that varies in thickness along vessel</li> </ul>
Retinal Vasculitis. What else looks like it?
<ul> <li><a>Silver-wiring</a> in chronic hypertension, where arterial wall is so thickened that red blood column is obliterated, BUT...in vasculitis you should see blood column unless vessel is occluded</li> <li>Attenuation of retinal nerve fiber layer from optic neuropathy </li> <li><a>Old retinal artery occlusion</a></li></ul>
Retinal Vasculitis. How do you manage it?
<ul> <li>Interpret this finding as sign of retinal vascular inflammation and think of diseases that do this</li> <li>Refer to ophthalmologist non-urgently unless symptoms are new and marked<br></br> </li> </ul>
Retinal Vasculitis. What will happen?
<ul> <li>Vasculitis may be restricted to eye, but more commonly it affects vessels in other tissues, so...</li> <li>Patient needs systemic work-up</li> <li>In retina, vessels can become occluded and cause blindness unless treatment undertaken</li> </ul>
Roth Spot. What is it?
<ul> <li>Cotton wool spot surrounded by hemorrhage, representing retinal microinfarct that bled</li> <li>Not specific for endocarditis</li><li>Many conditions cause this, including hypertension, diabetes, blood dyscrasia, HIV, bacterial endocarditis, connective tissue diseases, abusive head trauma in infants</li></ul>
Roth Spot. How does it appear?
<ul><li><a>Small flame-shaped hemorrhage with white spot in its center</a></li> </ul>
Roth Spot. What else looks like it?
<ul> <li>If you do not see white center, you will call this <a>retinal hemorrhage</a></li> </ul>
Roth Spot. How do you manage it?
<ul> <li>Interpret this as sign of small vessel occlusive disease of many causes</li> <li>Refer non-urgently to ophthalmologist for confirmation</li> </ul>
Roth Spot. What will happen?
<ul> <li>Roth spots do not usually affect vision, but they reflect systemic illness, including bacterial endocarditis, that could have dire consequences if not treated</li> </ul>
Subretinal Hemorrhage. What is it?
<ul> <li>Bleeding under retina in macular region</li> <li>Caused by new choroidal blood vessels that have burrowed into retina</li> <li>Most often found in <a>wet form of age-related macular degeneration</a></li> <li>Partly preventable by intravitreal injections of anti-vascular endothelial growth factor (VEGF) agents</li> </ul>
Subretinal Hemorrhage. How does it appear?
<ul> <li>Sudden painless loss of vision</li> <li>Red or purple or brown discoloration of retina in macular region</li></ul>
Subretinal Hemorrhage. What else looks like it?
<ul> <li><a>Choroidal tumor</a>, BUT...usually does not cause sudden loss of vision</li> <li>To learn more about retinal hemorrhages and their causes, check out <a>Retinal Hemorrhages</a></li> </ul>
Subretinal Hemorrhage. How do you manage it?
<ul> <li>Refer to ophthalmologist urgently if visual loss was recent</li> </ul>
Subretinal Hemorrhage. What will happen?
<ul> <li>Subretinal hemorrhages can recur frequently and lead to further loss of vision</li> <li>Intravitreal injections of anti-vascular endothelial growth factor (VEGF) agents can reduce frequency of hemorrhage</li> </ul>
Terson Syndrome. What is it?
<ul><li>Hemorrhagic retinopathy associated with subarachnoid and cerebral hemorrhage</li> <li>Bleeding usually surrounds optic disc, but...</li> <li>May break into vitreous cavity</li> <li>Caused by sudden marked elevation of intracranial pressure that bursts retinal veins</li> <li>Occurs immediately</li> <li>May be confused with papilledema, central retinal vein occlusion</li> <li>Hemorrhages usually resolve in months, but...</li> <li>May persist if have broken into vitreous, so that...</li> <li>Vitrectomy may be necessary to restore vision</li> </ul>
Terson Syndrome. How does it appear?
<ul> <li><a>Flame hemorrhages that surround optic disc</a>, sometimes obscuring it</li> <li>May also break into vitreous cavity so that retina hard to visualize </li> <li>Patient complains of reduced vision</li> <li>Usually affects both eyes, but often asymmetrically</li> </ul>
Terson Syndrome. What else looks like it?
<ul> <li>Traumatic avulsion of optic nerve, but should be history of direct impact on eye </li> <li><a>Central retinal vein occlusion</a>, but would not occur in this context</li> <li><a>Papilledema</a>, but not this hemorrhagic</li> <li>Vitreoretinal shear injury in <a>abusive head trauma</a>, but this occurs only in children under age 18 months </li></ul>
Terson Syndrome. How do you manage it?
<ul> <li>Refer patient with subnormal vision in subarachnoid or cerebral hemorrhage once stabilized</li> </ul>
Terson Syndrome. What will happen?
<ul> <li>No treatment for at least 6 months to allow for spontaneous resolution of vitreous hemorrhage</li> <li>Vitrectomy for persisting vitreous hemorrhage provided no other cause of disabling vision loss</li> </ul>
