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RETINA 01 > RYAN VOLUME 1 - FLUORESCEIN ANGIOGRAPHY > Flashcards

RYAN VOLUME 1 - FLUORESCEIN ANGIOGRAPHY Flashcards

1
Q

WHAT PRINCIPLE IS FA BASED ON? HOW TO EXPLAIN IT?

A

LUMINESCENCE - SPONTANEOUS EMISSION OF LIGHT FROM ANY SOURCE OTHER THAN HEAT AND OCCURS WHEN ENERGY IS ABSORBED AND THEN EMMITTED AT ANOTHER FREQUENCY.

LIGHT IS ABSORBER -> FREE ELECTRONS ELEVATED INTO HIGHER ENERGY STATES -> ENERGY REEMITTED BY SPONTANEOUS DECAY INTO LOWER ENERGY GROUND STATES.

ALWAYS A SHIFT FROM A SHORTER WAVELENGHT (MORE ENERGY) TO A LONGER WAVELENGHT (LESS ENERGY).

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2
Q

WHAT IS FLUORESCENCE?

A

A FORM OF LUMINESCENCE. IT IS MAINTAINED ONLY BY CONTINUOUS EXCITATION. EMISSION STOPS AS SOON AS EXCITATION STOPS. IT DOES NOT HAVE AN AFTERGLOW.

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3
Q

WHAT IS THE SODIUM FLUORESCEIN?

A

IT IS A HYDROCARBON THAT ABSORBS LIGHT ENERGY BETWEEN 465 - 490 nm (BLUE) AND FLUORESCES AT 520 - 530 nm (GREEN - YELLOW).

C20H12O5NA
376.27 DALTONS

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4
Q

HOW MUCH SODIUM FLUORESCEIN DYE IS FREE AND HOW MUCH IS BOUND?

A

80% IS BOUND.
20% IS FREE. THIS IS THE PART THAT EMITS FLUORESCENCE.

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5
Q

WHAT IS PSEUDOFLUORESCENCE?

A

IT OCCURS WHEN NONFLUORESCENT LIGHT PASSES THROUGH THE ENTIRE FILTER SYSTEM - WHEN BLUE LIGHT REFLECTED FROM THE NONFLUORESCENT FUNDUS STRUCTURES PENETRATES THE GREEN-YELLOW FILTER.

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6
Q

HOW TO AVOID PSEUDOFLUORESCENCE?

A

CAREFULLY MATCHING THE EXCITATION (BLUE) AND BARRIER (GREEN-YELLOW) FILTERS SO THAT THE OVERLAP OF LIGHT BETWEEN THEM IS MINIMAL.

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7
Q

SODIUM FLUORESCEIN DOSE

A

500MG
- 10mL 5%
- 5mL 10%
- 3mL 25% (750 mg)

GREATER VOLUME - LONGER INJECTION TIME REQUIRED
SMALLER VOLUME - THE DYE MAY REMAIN IN THE VENOUS DEAD SPACE BETWEEN ARM AND HEART.

ORAL INTAKE
25 mg/kg
IMAGES TAKEN AFTER 40 - 60 min

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8
Q

ELIMINATION OF SODIUM FLUORESCEIN

A

LIVER AND KIDNEYS WITHIN 24 HOURS.
KIDNEY DISEASE AND DIALYSIS ARE NOT CONTRAINDICATIONS.
YELLOWISH SKIN AND URINE UP TO 24H.

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9
Q

SIDE EFFECTS AND COMPLICATIONS OF SODIUM FLUORESCEIN

A
  • EXTRAVASATION / LOCAL TISSUE NECROSIS - RARE
  • ARTERIAL INJECTION
  • NAUSEA - MOST FREQUENT. 5% OF PATIENTS (30 SEC AFTER THE INJECTION).
  • VOMITING. 0.3 - 0.4% OF PATIENTS (40 - 50 SEC AFTER THE BEGGINING OF THE EXAM -INITIAL IMAGES ARE ALREADY TAKEN. SLOW INJECTION TO AVOID IT).
  • VASOVAGAL REACTION
  • ALLERGIC REACTION (HIVES AND ITCHING 2 MIN - 15 MIN) / ANAPHYLAXIS
  • NERVE PALSY
  • NEUROLOGIC - SEIZURES
  • TROMBOPHLEBITIS
  • PYREXIA
  • DEATH ( RISK 1 IN 220.000)
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10
Q

BREASTMILK VS FLUORESCEIN

A

FOUND UP TO 72 HOURS AFTER INJECTION.
IF NECESSARY, PUMP-AND-DUMP STRATEGY FOR 96 HOURS.

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11
Q

WHAT IS THE OPTOS SYSYTEM?

A

ULTRA-WIDEFIELD 200 DEGREES
ELLIPSOID MIRROR. CONFOCAL LASER (NOT A FLASH. NO TRUE COLLORS)
UP TO 82% OF THE RETINA WITH A SINGLE SCAN

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12
Q

WHAT IS THE SPECTRALIS ULTRA -WIDE SYSYTEM?

A

MODULE FOR THE SPECTRALIS. 102 DEGREES.
INTERCHANGEABLE LENSES
HIG-CONTRAST, UNDISTORTED IMAGES
IMPROVED VISUALIZATION OF SUPERIOR AND INFERIOR RETINA.

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13
Q

HOW TO INJECT FLUORESCEIN?

A

23 - 25 GAUGE NEEDLE. ANTECUBITAL VEIN // BACK OF THE HAND // SIDE OF THE WRIST.

COORDINATED WITH THE PHOTOGRAPHY PROCESS.
PREINJECTION PIC.
FIRST PIC WHEN INJECTION STARTS
SECOND PIC WHEN INJECTION ENDS

SOLWER INJECTION (4 -6 SECONDS) IS PREFERABLE.

INJECTION STARTS - TAKE A CONTROL PICTURE. THE TIMER STARTS COUNTING.

INITIAL-TRANSIT PHOTOGRAPHS AFTER THE BEGINNING OF THE INJECTION 8 SECONDS IN YOUNG AND 12 SECONDS IN OLDER PATIENTS.
THEN, RAPID SUCESSION EVERY 1.5 - 2 SECONDS.

20 - 30 SECONDS - PHOTOGRAPH OF THE MACULA AND OPTIC DISC OF THE FELLOW EYE

LATE PICS AT 5 - 10 MIN

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14
Q

INNER AND OUTER RETINA. HOW TO SPLIT?

A

INNER VASCULAR: ILM –> INNER NUCLEAR LAYER
- LARGER ARTERIES AND VEINS: NERVE FIBER LAYER
- SUPERFICIAL RETINAL CAPILLARIES: GANGLION CELL LAYER
- DEEP RETINAL CAPILLARIES: INNER NUCLEAR LAYER

OUTER AVASCULAR: OUTER PLEXIFORM LAYER/HENLE -> RODS AND CONES/RPE
- EXSUDATION IS FOUND IN OUTER PLEXIFORM AND INL.
- RPE IS FIRMLY ATTACHED TO THE BRUCH’S MEMBRANE.
- FLUORESCEIN PASSES FREELY FROM THE CHORIOCAPILLARIS AND BRUCH’S MEMBRANE, BUT NOT THROUGH THE RPE.

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15
Q

WHAT IS THE TRIANGULAR AMALRIC SYNDROME?

A

OCCLUSION OF THE SHORT POSTERIOR CILIARY ARTERIES OR THE LONG POSTERIOR CILIARY ARTERIES. IT CREATES WEDGE SHAPE INFARCTION AREAS NEAR THE MACULA. THE APEX IS DIRECTED TO THE FOVEA.

CAN BE ASSOCIATED WITH GIANT CELL ARTERITIS.

LPCA ALSO PERFUSES THE GREATER CIRCLE OF THE IRIS.

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16
Q

WHAT IS THE SIZE OF A CHORIOCAPILLARIS LOBULE?

A

1/4 - 1/2 DISC DIAMETER.
EACH IS FED BY A PRECAPILARY ARTEIOLE ORIGINATED FROM A SPCA.

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17
Q

HOW MANY VORTEX VEINS ARE THERE?

A

FOUR TO SEVEN

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18
Q

WHAT ARE THE LAYERS OF THE FOVEA?

A

FOUR LAYERS:
- ILM
- OPL / HENLE’S
- ONL
- RODS AND CONES

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19
Q

NORMAL HYPOFLUORESCENCE IN THE CENTER OF THE MACULA. WHY?

A

TALLER RPE CELLS (MORE COLUMNAR), GREATER CONCENTRATION OF MELANIN GRANULES; PRESENCE OF XANTHOPHYLL (IN HFL); CAPILLARY-FREE ZONE 400 - 500mm IN DIAMETER.

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20
Q

HOW IS THE OPTIC NERVE HEAD SUPPLIED?

A

TWO CIRCULATORY SYSTEMS:
- RETINAL
- POSTERIOR CILIARY ARTERIES

THERE ARE WIDESPREAD ANOSTOMOTIC CHANNELS

21
Q

IN 12% OF PERSONS, THE CENTRAL RETINAL ARTERY ARISES FROM THE CILIARY ARTERY. WHAT IS A CLINICAL CONSEQUENCE OF THAT?

A

A SINGLE SITE OF OBSTRUCTION CAN CAUSE:
- CHOROIDAL INFARCTION
- ANTERIOR ISCHEMIC OPTIC NEUROPATHY
- CENTRAL RETINAL ARTERIA OCCLUSION

22
Q

DOES FLUORESCEIN APPEAR SIMULTANEOUSLY IN THE OPTIC NERVE HEAD AND THE CHOROID?

A

YES. BECAUSE IT IS MOSTLY IRRIGATED BY THE CILIARY SYSTEM.

23
Q

WHAT ARE THE “OPTOCILIARY SHUNT VESSELS”?

A

A MISNOMER. THEY ARE RETINOCILIARY VEINS - COLLATERAL VEINS THAT EMANATE FROM THE RETINA TO THE CHOROID.

24
Q

NORMAL FLUORESCEIN ANGIOGRAM INITIAL TIMING

A

FIRST EVIDENCE OF PERFUSION IN CHOROID IN 10 - 12 SECONDS (YOUNGS) AND 12 - 15 (ELDERLY)
20 - 25 - VERY BRIGHT FOR ABOUT 5 SEC. THIS IS THE EXTREME CHOROID FLUORESCENCE

25
Q

HOW IS THE FLUORESCENCE PATTERN OF THE CILIORETINAL ARTERY? AND THE CRA?

A

IT DISPLAYS FLUORESCENCE SIMULTANEOUSLY WITH THE CHOROIDAL FLUSH.

THE CENTRAL RETINAL ARTERY WILL FLUORESCE 1 TO 3 SECONDS AFTER CHOROIDAL FLUORESCENCE.

26
Q

HOW DOES THE DENSITY OF THE EPR INFLUENCE THE EXAM?

A

DENSER RPE: LESS CHOROIDAL FLUORESCENCE. GREATER CONTRAST AND VISIBILITY OF THE RETINAL VASCULATURE.

27
Q

SUMMARIZE FA PHASES

A
  • CHOROIDAL FILLING AFTER 10 - 15 SEC (8 IN VERY YOUNG) AFTER INJECTION
  • INITIAL RETINAL FILLING AFTER 1- 3 SEC
  • EARLY ARTERIOVENOUS PHASE
  • LATE ARTERIOVENOUS PHASE - LAMINAR VENOUS
  • MAXIMUM PEAK AT 30 SEC
  • RECIRCULATION PHASE FOR 3 - 5 MINUTES
  • NO CONTRAST AFTER 10 MIN
28
Q

IN THE LATE PHASES, CONSIDERING A LIGHTLY PIGMENTED RPE, WHAT STRUCTURES CAN BE SEEN IN A STAINING PATTERN?

A

BRUCH’S MEMBRANE, THE CHOROID, THE SCLERA

29
Q

CAUSES OF HYPOFLUORESCENCE

A
  • BLOCKED FLUORESCENCE
  • VASCULAR FILLING DEFECT
30
Q

CAUSES OF BLOCKED RETINAL FLUORESCENCE

A
  • CORNEA, ANT SEGMENT, LENS, VITREOUS OPACITIES (ASTEROID HYALOSIS MAY IMPAIR MORE THE COLOR PHOTOGRAPHY THAN THE FA DUE TO THE NEUTRALIZATION OF THE EMISSION/BARRIER FILTERS).
  • HEMORRAGE
    – SUB-ILM: BLOCKS ENTIRE RETINA
    – NFL: FLAME SHAPED, BLOCKS DEEPER CAPILLARIES BUT ONLY PARTIALLY BLOCKS LARGER RETINAL VESSELS
  • MYELINATED FIBERS - PARTIAL BLOCKAGE (HEMORRAGE IS TOTAL)
  • COTTON WOOL SPOTS
  • PURTSCHER’S RETINOPATHY (BLOCKAGE + VASCULAR FILLING DEFECT)
31
Q

CAUSES OF BLOCKED RETINAL FLUORESCENCE

A
  • CORNEA, ANT SEGMENT, LENS, VITREOUS OPACITIES (ASTEROID HYALOSIS MAY IMPAIR MORE THE COLOR PHOTOGRAPHY THAN THE FA DUE TO THE NEUTRALIZATION OF THE EMISSION/BARRIER FILTERS).
  • HEMORRAGE
    – SUB-ILM: BLOCKS ENTIRE RETINA
    – NFL: FLAME SHAPED, BLOCKS DEEPER CAPILLARIES BUT ONLY PARTIALLY BLOCKS LARGER RETINAL VESSELS
  • MYELINATED FIBERS - PARTIAL BLOCKAGE (HEMORRAGE IS TOTAL)
  • COTTON WOOL SPOTS
  • PURTSCHER’S RETINOPATHY (BLOCKAGE + VASCULAR FILLING DEFECT)
32
Q

THE FIVE CATEGORIES OF HYPERFLUORESCENCE

A
  • PREINJECTION FLUORESCENCE
  • TRANSMITTED FLUORESCENCE (EARLY)
  • ABNORMAL VESSELS (EARLY)
  • LEAKAGE (LATE)
  • STAINING
33
Q

THE TWO CAUSES OF PREINJECTION FLUORESCENCE

A
  • AUTOFLUORESCENCE
    — OPTIC DISC DRUSEN
    — ASTROCITIC HAMARTOMA
  • PSEUDOFLUORESCENCE
    — BLUE EXCITATION AND GREEN EMISSION FILTERS OVERLAP
34
Q

MAJOR CAUSE OF TRANSMITTED HYPERFLUORESCENCE

A

RPE ATROPHY

NOTE: IF THE CHORIOCAPILLARIS DOES NOT FILL, A DEPIGMENTED AREA OF RPE WILL NOT FLUORESCE

35
Q

BASIC CHARACTERISTICS OF TRANSMITTED HYPERFLUORESCENCE

A
  • APPEARS EARLY, COINCIDENTAL WITH CHOROIDAL FILLING
  • HYPERFLUORESCENCE INCREASES AS DYE INCREASES IN THE CHOROID
  • STABLE IN SIZE AND SHAPE
  • DISAPPEARS AS THE CHOROID EMPTIES OF DYE
36
Q

SIX MORPHOLOGIC CATEGORIES OF ABNORMAL VASCULAR FLUORESCENCE

A
  • TORTUOSITY AND DILATION
  • TELANGIECTASIA
  • ANEURYSMS
  • ANASTOMOSIS
  • NEOVASCULARIZATION
  • TUMOR VESSELS
37
Q

DIFFERENCES IN TYPE 1 AND 2 MNV

A

MNV TYPE 1
- HOT SPOT AT THE EDGE OF EDGE OF A PED.
- STIPPLED FLUORESCENCE ASSOCIATED WITH A PED.

MNV TYPE 2
- LACY / SPOKE-WHEEL PATTERN

38
Q

BARRIERS LOST IN A CASE OF LEAKAGE

A

TIGHT JUNCTIONS OF THE RETINAL VASCULAR ENDOTHELIUM AND/OR ZONULAE OCCLUDENTES OF THE RPE.

39
Q

THREE MAJOR CAUSES OF VITREOUS LEAKAGE

A
  • NEOVASCULARIZATION (COTTON-BALL APPEARENCE)
  • INTRAOCULAR INFLAMMATION (GENERALIZED, DIFFUSE WHITE HAZE)
  • INTRAOCULAR TUMORS (LOCALIZED OVER THE TUMOR).
40
Q

CAUSES OF DISK LEAKAGE

A

INFLAMMATORY DISEASES CAUSING PAPILLITIS
CRVO
SWELLING OF THE DISC HEA (HIGH INTRACRANIAL PRESSURE)
AION - SECTORAL PATTERN OF LEAKAGE

41
Q

CHARACTERISTICS OF CYSTOID SPACES

A

THEY LEAK IN MULTIPLE WAYS:
CYSTOID SPACES MAY FILL SLOWLY AND BE VISIBLE ONLY IN LATE PHASES, FLUID MAY BLOCK FLUORESCENCE EARLY IN THE ANGIOGRAM.

CYSTOID SPACES CAN FILL RAPIDLY, EVEN WITHIN ONE MINUTE.

42
Q

THREE SITUATIONS IN WHICH LARGE RETINAL VESSELS CAN LEAK

A
  • INFLAMMATION / VASCULITIS
  • VITREORETINAL TRACTION
  • OCCLUSION
43
Q

WHAT’S THE DIFFERENCE BETWEEN POOLING AND LEAKAGE?

A

POOLING IS DEFINED AS LEAKAGE INTO A DISTINCT ANATOMIC SPACE. LEAKAGE IS FLUORESCEIN PRESENT DIFFUSELY INTO A TISSUE PLANE.

44
Q

DIFFERENCES BETWEEN POOLING OF A PED AND A NEUROSENSORY RETINAL DETACHMENT

A

PED
- OBTUSE / LARGE ANGLE OF PED (RPE ADHERES FIRMLY TO THE COLLAGENOUS FIBERS OF BRUCH’S MEMBRANE)
- EASIER RECOGNITIOM
- LIGHT ORANGE RIM MAY BE NOTED
- POOLING MORE RAPID AND INTENSE (DIRECT CHOROIDAL LEAKAGE)

NEUROSENSORY RETINAL DETACHMENT
- ACUTE OR SMALLER ANGLE
- NOT WELL DEMARCATED IN FA IMAGING
- SLOWER POOLING

45
Q

DRUSEN / DRUSENOID PEDs PATTERN

A

THEY MAY SHOW LATE HYPERFLUORESCENCE AND POOLING.

46
Q

FOUR TYPES OF LATE STAINING IN NORMAL EYES

A
  • DISC MARGINGS (SURROUNDING CHORIOCAPILLARIS)
  • LAMINA CRIBROSA
  • SCLERAL CRESCENT (RPE TERMINATES OR RECEDES AWAY FROM THE DISC MARGIN)
  • SCLERA (WHEN RPE IS LIGHTLY PIGMENTED)
47
Q

RPE TEAR GRADING (Sarraf et al)

A

1) DIAMETER < 200 MICRA
2) DIAMETER BETWEEN 200 MICRA AND 1 DD
3) DIAMETER > 1 DD
4) DIAMETER > 1 DD THAT INVOLVES THE FOVEA CENTER

48
Q

BEHAVIOR OF THE DRUSEN IN FA

A
  • EARLY HYPERFLUORESCENCE (BY TRANSMISSION): DEFECTS OF THE RPE OVERLYING THE DRUSEN.
  • FLUORESCENCE OF SMALLER DRUSEN DIMINISHES AS THE DYE EXITS THE CHOROIDAL CIRCULATION
  • LARGE DRUSEN MAY DISPLAY LATE STAINING (LARGER DRUSEN, MORE LIKELY IT WILL STAIN)
  • DRUSENOID PEDS CAN POOL AND STAIN WITH SMOOTH EDGES
49
Q

HOW DO SCARS STAIN?

A

FIBROVASCULAR SACRAS (DISCIFORM SCAR)
- EARLY HYPERFLUORESCENCE. LATE LEAKAGE. LATE STAINING.

FIBROCELLULAR SCARS
- EARLY BLOCKAGE. LATE STAINING.

RETINA 01 (5 decks)

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