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