Retina tests Flashcards
FA - expansile dot
FA - patchy delayed choroidal filling
Expansile dot leakage from the choriocapillaris into the subretinal space occurs in central serous chorioretinopathy (along with the “chimney stack” leakage pattern).
Patchy, delayed choroidal filling is typical of choroidal ischemia in giant cell arteritis although can occur in other choroidopathies such as hypertensive choroidopathy or Wegener granulomatosis-associated choroidopathy.
ERG
- a-wave: cones and rods (outer PR layer)
- b-wave: Muller and bipolar cells (inner retina) = positive (upgoing) deflection,
- c-wave: RPE and PRs
measures the mass response of the photoreceptors and cannot be used to estimate visual acuity
Cone function can be measured with a 30-Hz flicker response since rods do not respond over 20-Hz and also with photopic ERG, which is performed when the eye is in the light-adapted state.
To measure rod function, one can perform an ERG with the eye in the dark-adapted state (i.e. scotopic ERG).
FA pooling
Pooling is marked by hyperfluorescence that increases in size and intensity progressively as dye enters a closed space (such as fluorescein leakage into a retinal pigment epithelial detachment). Once the closed space fills, the area of hyperfluorescence remains stable in size differentiating pooling from leakage.
FA staining
Staining is marked by uptake of fluorescein into structures such as drusen or the optic disc. Staining causes hyperfluorescence that maintains its intensity late into the FA but without an increase in the area of hyperfluorescence over time.
FA leakage
Leakage is marked by hyperfluorescence that increases in size and intensity over time corresponding to extravasation of dye from leaking blood vessels. Choroidal neovascular membranes and neovascularization are examples of lesions that leak on FA.
FA window defect
Window defects are usually related to damage to the retinal pigment epithelium causing increased visibility of the underlying hyperfluorescent choroid. Geographic atrophy is a classic example of a lesion that exhibits window defect related hyperfluorescence. Hyperfluorescence from a window defect is usually more prominent EARLY IN THE FA and DECLINES WITH TIME corresponding to the concentration of dye in the choroid.
ICG
ICG is almost completely protein-bound (>95%) and thus does not diffuse well through the fenestrations of the choriocapillaris. In other words, ICG mostly stays within the choroidal circulation which makes ICG angiography useful for imaging of the choroidal circulation. ICG has <5% the fluorescence of fluorescein dye and fluoresces in the near-infared range. It is this longer wavelength that allows ICG to fluoresce better through blood, lipid, fluid, and pigment compared to fluorescein.
Another advantage of ICG angiography is that it is associated with a lower rate of side effects (e.g. nausea, vomiting) compared to FA. You should ask any patient undergoing ICG angiography if they are allergic to iodide or shellfish since ICG contains 5% iodide. Since ICG is metabolized via the liver, one should be cautious when administering this dye in patients with a history of liver disease.
FA SE
incidence of nausea/vomiting/syncope from FA is approximately 10%.
Other notable possible side effects are:
urticarial (anaphylactoid) reactions - 1%
cardiovascular shock (anaphylactic) - <1:100,000
temporary (6-12 hours) yellowing of skin and conjunctiva - all patients
You should also warn your patients that their urine may appear bright orange-yellow for 24-36 hours after FA.
ERG reduced and delayed of cone or rod b-wave
Reduction and delay of cone (or rod) b-waves signifies damage to cells diffusely THROUGHOUT the retina
Occurs in:
dystrophic dz (RP)
widespread ischemic disorders (CRVO)
diffuse infection/inflammation (syphilis)
Reduced b-wave amplitude with normal shape/timming of waveform
Sector RP
EOG (subnormal) but normal ERG
classic finding in Best disease
seen occasionally in various adult-onset pattern dystrophies
RP’s ERG and EOG
both are subnormal
Rubella EOG
RPE is diffusely affected but normal EOG
negative ERG
“negative ERG” with a near normal A-wave but a markedly diminished B-wave
See in CSNB and retinoschisis and MAR
basis of the electrooculogram (EOG).
Apical surface has the Na+K+-ATPase. This ATPase transports ions from the subretinal space into the RPE cells. The net flow of ions across this apical surface creates an electrical potential that can be measured.
suspicion of a cone-rod dystrophy. You have an ERG. What else do you need to correctly interpret the ERG?
You need a kinetic visual field, like the GVF, to correctly interpret the results of the ERG, especially in patients with a predominantly cone loss.
Fluorescein sodium absorbs/emits
Absorbs at 465-490nm (blue)
Emit at 520-530nm (green)
80% bound to plasma protein
90% renal excretion
Fluorescein phases
Phases Choroidal phase (10-15s) Arterial phase (15-18s) Early arteriovenous phase Arteriovenous phase (20-25s) Recirculation phase (30+s) Late phase (fluorescein leaves retinal circulation by 10min)
Fluorescein Hyperfluorescence DDx
Autofluorescence (from lipofuscin) Transmission defect Leaking (increasing blurred border) Pooling (accumulate in anatomic space) Staining (fixed margins)
Fluorescein Hypofluorescence DDx
Hypofluorescence
Blocked fluorescence
Filling Defect
ICG
Absorbs at 805m; Emit at 835nm
98% bound to albumin (stays in choroidal vessels, so better for choroidal circulation)
5% iodine – avoid if shellfish allergy
OCT
Time domain = higher bandwidth = higher axial res
Frequency/Spectral domain = faster, better signal-to-noise ratio
What is tested by Early receptor potential?
Early receptor potential?
Outer segment of photoreceptor
What is tested by A-wave?
A-wave?
Photoreceptors
