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Ocular Disease 4 > Lecture 3/6 - acquired macular diseases > Flashcards

Lecture 3/6 - acquired macular diseases Flashcards

1
Q

what causes central serous chorioretinopathy (CSR)?

A

idiopathic = altered barrier/deficient RPE pump or leaking choriocapillaris (retina + choroid problem)

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2
Q

what is the pathophysiology of CSR?

A

fluid accumulates under RPE - breaks through and accumulates under the retina - causes an RPE/retina detachment (localized and well defined)

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3
Q

who typically gets CSR?

A

healthy 25-55 year old male, white/hispanic/asian, Type A personality, possible stress etiology

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4
Q

what are the associations with CSR?

A

exogenous or endogenous steroids, cushings syndrome, organ transplants, SLE, HTN, sleep apnea, GERD, psych meds, pregnancy

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5
Q

what are the signs/symptoms of CSR?

A

sudden onset blurred/dim vision (hyperopic shift), micropsia, metamorphopsia, paracentral scotoma, decreased color vision, VA 20/20 - 20/200, may have headache, unilateral or asymmetric bilateral

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6
Q

what are the 3 patterns of CSR in FA?

A

expansile dot pattern (most common), smokestack pattern (most characteristic), and diffuse pattern

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7
Q

what is seen on an OCT of CSR?

A

increased choroidal thickness and fluid under the RPE/retina (if there are clusters of deposits, it has been there awhile)

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8
Q

what is seen with fundus autofluorescence (FAF) in CSR?

A

pigment mottling in the area of RPE disturbance and altered autofluorescence corresponding to site of focal RPE leak (precipitates)

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9
Q

what is seen with ICG in CSR?

A

“washout pattern” in late phase - helps distinguish atypical diffuse CSR in older patients from occult CNVM and idiopathic polypoidal choroidal vasculopathy

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10
Q

what is the prognosis for CSR?

A

generally good except in chronic, recurrent cases and bullous CSR
most (80-90%) have spontaneous resolution in 3-4 months

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11
Q

what treatment is available for CSR?

A

observe 3-6 months - then laser photocoagulation at leakage or PDT if it is needed
RTC 3-4 weeks after laser to monitor for CNVM

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12
Q

what are signs of chronicity in CSR?

A

cystic changes (microcavities) in neurosensory retina or widespread RPE abnormalities

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13
Q

what is an optic nerve pit?

A

small, hypopigmented, yellow/white, oval/round, excavated colobomatous defect

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14
Q

where is an optic nerve pit usually located?

A

inferior temporal at disc margin - mostly unilateral and asymptomatic

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15
Q

what can an optic nerve pit cause?

A

serous macular detachments - can be cerebral spinal fluid or liquid vitreous

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16
Q

what will an OCT show for a serous macular detachment caused by an optic nerve pit?

A

macular schisis and SRF (subretinal fluid)

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17
Q

what is the treatment for a serous macular detachment caused by an optic nerve pit?

A

laser along the edge of the optic nerve pit forming a barrier to fluid, use a gas bubble or vitrectomy

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18
Q

what is an epiretinal membrane (ERM)?

A

semitranslucent, avascular, fibrocellular membrane = covers the internal limiting membrane (ILM)

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19
Q

what cells are involved with an ERM?

A

proliferating glial (astrocytes or muller) cells, hyalocytes, fibroblasts, myofibroblasts and macrophages

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20
Q

what causes an ERM?

A

most common is idiopathic = abnormal vitreoretinal interface with a PVD or vitreous separation after age 50 (10-20% are bilateral and asymmetric)

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21
Q

what are secondary causes of an ERM?

A

retinal vascular occlusions, uveitis, trauma, intraocular surgery, retinal breaks

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22
Q

how do you know if a patient with a PVD will develop an ERM?

A

it depends on where the plane of the vitreous is located - if the hyalocytes are detached with the vitreous they die, if they stay they proliferate on ILM

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23
Q

what are the grading classifications of an ERM?

A

mild/cellophane (no metamorphopsia), moderate (retinal striae), severe (macular pucker)

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24
Q

what are the symptoms of an ERM?

A

micropsia, macropsia, metamorphopsia, decreased VA, diplopia, floaters, or asymptomatic

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25
Q

what are the signs of an ERM?

A

retinal vessel traction (straightening of the perimacular vessels), optic nerve staining on FA, intra-retinal hemorrhages, superficial retinal whitening CWS, pseudohole

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26
Q

what is the treatment for an ERM?

A

monitor with amsler if mild, only treat if vision is less than 20/50 or there is intolerable distortion = PPV + ERM peel

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27
Q

what is vitreomacular traction syndrome (VMT)?

A

an incomplete separation of the posterior vitreous to the posterior pole at the macula

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28
Q

what causes a VMT?

A

a partial PVD with cellular proliferation

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29
Q

what are the signs of a VMT?

A

abnormal opacities in central vitreous, traction over the macular and optic nerve, similar signs to ERM without an ERM (retina is distorted, cystic, tented with shallow detachment)

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30
Q

what is seen on FA with VMT?

A

macular vessels leak, disc distortion, early CME

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31
Q

what is the treatment for VMT?

A

same as ERM - only if the VA is less than 20/50 or severe distortion, may have spontaneous resolution

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32
Q

what causes an idiopathic macular hole?

A

tractional forces at early PVD (older patients, F>M)

33
Q

what are the stages of an idiopathic macular hole?

A

stage 0/premacular hole, stage 1a foveolar detachment, stage 1b foveal detachment, stage 2 full thickness (less than 400um), stage 3 fully developed (greater than 400um) +/- operculum and stage 4 fully developed hole + PVD

34
Q

what happens when an idiopathic macular hole is at stage 0?

A

perifoveal PVD, subtle loss of foveal depression and normal VA (most do not progress)

35
Q

what happens when an idiopathic macular hole is at stage 1a?

A

loss of foveal depression + small yellow spot (pseudocyst with perifoveal vitreous detachment)

36
Q

what happens when an idiopathic macular hole is at stage 1b?

A

loss of foveal depression + small yellow ring

37
Q

what happens when an idiopathic macular hole is at stage 2?

A

dehiscence as a tractional break “roof” of pseudocyst,

38
Q

what happens when an idiopathic macular hole is at stage 3?

A

hole is >400um, rim is elevated/thickened, VA 20/40-20/200, posterior hyaloid attached to optic disc/detached from fovea, +/- operculum

39
Q

what happens when an idiopathic macular hole is at stage 4?

A

fully developed hole + complete PVD

40
Q

what is seen on the FA in an idiopathic macular hole?

A

window defect (loss of normal tissue that was blocking the macula)

41
Q

what is the management for an idiopathic macular hole?

A

spontaneous resolution in 50% of cases - no treatment if stage 1
stages 2-4 = surgery only if VA is less than 20/50 (vitrectomy + peel and gas bubble for positioning)

42
Q

what is ocular ischemic syndrome (OIS)?

A

rare, but vision-threatening, condition associated with severe carotid artery occlusive disease (stenosis or occlusion) leading to ocular hypoperfusion (slowly progressive VA loss)

43
Q

what is OIS associated with?

A

periorbital aching pain, amaurosis fugax, prolonged recovery after exposure to a bright light (post stress test)

44
Q

what is seen on slit lamp examination with OIS?

A

NVI, increased IOP, AC reaction

45
Q

what is it called if there is only posterior segment findings vs. anterior + posterior?

A

posterior = venous stasis syndrome

anterior + posterior = OIS

46
Q

who typically gets OIS?

A

older patients (50-70) M>F, associated with HTN, DM, CAD

47
Q

what are the OIS signs seen during DFE?

A

narrowed arteries, dilated but not very tortuous veins, unilateral (80%) microaneurysms and hemorrhages (deep, round, mid-periphery), NVD/NVE

48
Q

what is a differential diagnosis of OIS?

A

CRVO - this has normal artery pressure vs. OIS has low artery pressure and central retinal artery will collapse with gentle pressure

49
Q

what is seen on FA with OIS?

A

delayed choroidal filling, delayed arteriovenous transit time and prominent vascular staining (arteries)

50
Q

what is seen on ERG in OIS?

A

diminished amplitude of A and B waves = inner and outer retinal ischemia

51
Q

what is the etiology of OIS?

A

atherosclerosis, inflammatory conditions (Eisenmenger syndrome, giant cell arteritis, etc.)

52
Q

what is the treatment if the patient develops NVI in OIS (90% are blind within 1 year)?

A

full scatter PRP

53
Q

what is the treatment for OIS?

A

carotid artery stenting and endarterectomy

54
Q

what is purtscher retinopathy?

A

loss of vision after acute compression injuries to the thorax or head, unilateral or bilateral loss

55
Q

what are the signs of purtscher retinopathy?

A

large CWS, hemorrhages, retina edema surrounding the optic disc, APD

56
Q

what is seen on FA with purtscher retinopathy?

A

arteriolar obstruction and leakage

57
Q

what are some conditions associated with purtscher or purtscher-like retinopathy?

A

trauma, acute pancreatitis, amniotic fluid embolism, autoimmune diseases

58
Q

what is the pathophysiology of purtscher retinopathy?

A

injurry-induced complement activation - granulocyte aggregation and leukoembolization - arterial occlusion (especially peripapillary)
other causes = fat emboli from bone, air emboi

59
Q

what is valsalva or venous retinopathy?

A

increase in venous pressure - ruptured small superficial capillaries in the macula = hemorrhagic detachment of ILM

60
Q

what are the signs/symptoms of valsalva or venous retinopathy?

A

VA mildly reduced,vitreous hemorrhage or subretinal hemorrhage are possible

61
Q

what are the differential diagnoses for valsalva or venous retinopathy?

A

PVD and macroaneurysms

62
Q

what is seen on the OCT of valsalva or venous retinopathy?

A

it looks like a macular hole but the top layers are still intact

63
Q

what is hyperviscosity syndrome?

A

increased viscosity secondary to elevated protein levels = causes decreased flow and damage to vessels (leakage/ischemia)

64
Q

who typically gets hyperviscosity syndrome?

A

younger patients, athletes (symptoms do not match history - blood work is usually needed)

65
Q

what are the signs/symptoms of hyperviscosity syndrome?

A

CWS, exudates, CRVO is possible

66
Q

what conditions have high protein levels (hyperglobulinemia) seen in hyperviscosity syndrome?

A

waldenstrom’s, multiple myeloma, SLE, HIV, Rh+ve, rheumatoid arthritis

67
Q

when is HIV retinopathy seen?

A

70% in advanced disease, 40% in symptomatic intermediate stage HIV and 1% in asymptomatic HIV infection

68
Q

what distinguishes HIV retinopathy from CMV?

A

the CWS are smaller, superficial location, no progression and tendency to resolve over weeks-months

69
Q

what retinal findings are seen in HIV retinopathy?

A

CWS, hemorrhages (flame and blot), telangiectatic vascular changes and microaneurysms, areas of capillary non-perfusion (NVD/NVE), retinal vein and artery occlusions

70
Q

what does interferon retinopathy look like?

A

retinal hemorrhages (superficial, linear, patchy), CWS around optic disc, ischemia on FA, VA is usually unaffected, unilateral or bilateral

71
Q

what is atypical in interferon retinopathy?

A

BRVO, pre-retinal hemorrhage and VA affected

72
Q

when does interferon retinopathy show up?

A

2 weeks to 3 months after starting interferon therapy (incidence depends on initial dose = DM patients have a higher incidence/progression)

73
Q

what is the treatment for interferon retinopathy?

A

disappears spontaneously during therapy or rapidly after stopping therapy

74
Q

when is talc retinopathy seen?

A

usually with long term drug user - they develop collaterals in the lungs (venous and artery anastomose) and gets distributed in the retina

75
Q

what is Terson syndrome?

A

a vitreous, sub-ILM, or sub-hyaloid hemorrhage caused by an abrupt intracranial hemorrhage (blood in brain = subarachnoid or subdural hemorrhage)
between ages 30-50

76
Q

what causes terson syndrome?

A

possible an acute intracranial hemorrhage - acute rise in the intraocular venous pressure, peripapillary and retinal vessels rupture

77
Q

what is the treatment for terson syndrome?

A

vitrectomy if non-resolving (VA unaffected once the blood clears - spontaneously)

78
Q

what are the signs of child abuse syndrome?

A

periorbital ecchymosis, traumatic retinoschisis and retinal folds

79
Q

what causes the retinal damage in child abuse syndrome?

A

contrecoup forces from trauma, oscillating vitreous traction of formed vitreous

Ocular Disease 4 (6 decks)

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