Introduction

Fluorescein angiography (FA) should be performed only if the findings are likely to influence management.

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  Fluorescence is the property of certain molecules to emit light of a longer wavelength when stimulated by light of a shorter wavelength. The excitation peak for fluorescein is about 490 nm (in the blue part of the spectrum) – the wavelength of maximal absorption of light energy by fluorescein. Stimulated molecules will emit yellow–green light of about 530 nm ( Fig. 14.13 ).

  
  

  
  

  
  

  

  
  

  
  

  Excitation and emission of fluorescein

  
  
  
  
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  Fluorescein (sodium fluorescein) is an orange water-soluble dye that, when injected intravenously, remains largely intravascular (>70% bound to serum proteins). It is excreted in the urine over 24–36 hours.

  
  
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  FA involves photographic surveillance of the passage of fluorescein through the retinal and choroidal circulations following intravenous injection.

  
  
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  Outer blood–retinal barrier. The major choroidal vessels are impermeable to both bound and free fluorescein. However, the walls of the choriocapillaris contain fenestrations through which unbound molecules escape into the extravascular space, crossing Bruch membrane but on reaching the RPE are blocked by intercellular complexes termed tight junctions or zonula occludentes ( Fig. 14.14 ).

  
  

  
  

  
  

  

  
  

  
  

  The outer blood–retinal barrier (Z.O. = zonula occludentes; B.M. = Bruch membrane)

  
  
  
  
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  Inner blood–retinal barrier is composed principally of the tight junctions between retinal capillary endothelial cells, across which neither bound nor free fluorescein can pass; the basement membrane and pericytes play only a minor role in this regard ( Fig. 14.15A ). Disruption of the inner blood–retinal barrier permits leakage of both bound and free fluorescein into the extravascular space ( Fig. 14.15B ).

  
  

  
  

  
  

  

  
  

  
  

  Inner blood–retinal barrier. (A) Intact; (B) disrupted (E = endothelial cell; B.M. = basement membrane; P = pericyte)

  
  
  
  
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  Filters ( Fig. 14.16 )

  
  
  
  
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    Cobalt blue excitation filter. Incident white light from the camera is filtered so that blue light enters the eye, exciting the fluorescein molecules in the retinal and choroidal circulations.

    
    
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    Yellow–green barrier filter blocks any blue light reflected from the eye, allowing only yellow–green emitted light to pass.

  
  

  
  

  
  

  

  
  

  
  

  Principles of fluorescein angiography

  
  
  
  
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  Image capture in modern digital cameras uses a charge-coupled device (CCD). Digital imaging permits immediate picture availability, easy storage and access, image manipulation and enhancement. Modern devices also typically require a lower concentration of injected fluorescein to obtain high-quality images, with a correspondingly substantially lower incidence of adverse effects.

  
  
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  Contraindications

  
  
  
  
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    Fluorescein allergy is an absolute contraindication, and a history of a severe reaction to any allergen is a strong relative contraindication. Preventative anti-allergy pre-treatment may be helpful in some cases.

    
    
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    Other relative contraindications include renal failure (a lower fluorescein dose is used), pregnancy, moderate–severe asthma and significant cardiac disease.

    
    
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    Allergy to iodine-containing media or seafood is not a clear contraindication to FA or to indocyanine green angiography (ICGA).

  
  

Technique

Facilities must be in place to address possible adverse events. This includes adequate staffing, a resuscitation trolley that includes drugs for the treatment of anaphylaxis, a couch (or reclining chair) and a receiver in case of vomiting; significant nausea and vomiting, and probably other adverse reactions, are now much less common with the lower fluorescein concentrations required by modern digital cameras.

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  Adequate pharmacological mydriasis is important to obtain high-quality images; media opacity such as cataract may reduce picture quality.

  
  
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  The procedure is explained and formal consent taken. It is important to mention common and serious adverse effects ( Table 14.2 ), particularly the invariable skin and urine staining. As noted above, adverse effects are generally now much less common.

  
  
  
  

  Table 14.2

  
  

  Adverse events in fluorescein angiography

  
  

  
  
  
  
  

  Discoloration of skin and urine (invariable) Extravasation of injected dye, giving a painful local reaction (treat with cold compress) Nausea, vomiting (now rare with lower concentrations of fluorescein) Itching, rash Sneezing, wheezing Vasovagal episode or syncope (usually due to anxiety but sometimes to ischaemic heart disease) Anaphylactic and anaphylactoid reactions (1 : 2000 angiograms) Myocardial infarction (extremely rare) Death (1 : 220 000 in the largest study)

   
  
  
  
  
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  The patient should be seated comfortably in front of the fundus camera, and colour photographs, red-free (green incident light, to enhance red detail) and autofluorescence images taken as indicated.

  
  
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  An intravenous cannula is inserted; a standard cannula is often preferred rather than a less secure ‘butterfly’ winged infusion set. After cannulation, the line should be flushed with normal saline to check patency and exclude extravasation.

  
  
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  Fluorescein, usually 5 ml of a 10% solution, is drawn up into a syringe and injected over the course of 5–10 seconds, taking care not to rupture the cannulated vein ( Fig. 14.17 ).

  
  

  
  

  
  

  

  
  

  
  

  Injection and circulation of fluorescein

  
  
  
  
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  Oral administration at a dose of 30 mg/kg is an alternative if venous access cannot be obtained or is refused; a 5 ml vial of 10% (100 mg/ml) sodium fluorescein contains 500 mg, and pictures should be taken over 20–60 minutes following ingestion.

  
  
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  Images are taken at 1–2 second intervals initially to capture the critical early transit phases, beginning 5–10 seconds after injection, tapering frequency through subsequent phases.

  
  
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  With monocular pathology, control pictures of the opposite eye should be taken, usually after the initial transit phase has been photographed in the index eye.

  
  
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  If appropriate, images may be captured as late as 10–20 minutes.

  
  
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  Stereo images may be helpful to demonstrate elevation, and are usually taken by manually repositioning the camera sideways or by using a special device (a stereo separator) to adjust the image; these are actually ‘pseudostereo’, true stereo requiring simultaneous image capture from different angles.

Angiographic phases

Fluorescein enters the eye through the ophthalmic artery, passing into the choroidal circulation through the short posterior ciliary arteries and into the retinal circulation through the central retinal artery ( Fig. 14.18 ); the choroidal circulation fills about 1 second before the retinal. Precise details of the choroidal circulation are typically not discernible, mainly because of rapid leakage of free fluorescein from the choriocapillaris; melanin in the RPE cells also blocks choroidal fluorescence. The angiogram consists of the following overlapping phases:

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  The choroidal (pre-arterial) phase typically occurs 9–15 seconds after dye injection – longer in patients with poor general circulation – and is characterized by patchy lobular filling of the choroid due to leakage of free fluorescein from the fenestrated choriocapillaris. A cilioretinal artery, if present, will fill at this time because it is derived from the posterior ciliary circulation ( Fig. 14.19A ).

  
  

  
  

  
  

  

  
  

  
  

  Normal fluorescein angiogram. (A) Choroidal phase shows patchy choroidal filling as well as filling of a cilioretinal artery; (B) arterial phase shows filling of the choroid and retinal arteries; (C) arteriovenous (capillary) phase shows complete arterial filling and early laminar venous flow; (D) early venous phase shows marked laminar venous flow; (E) mid-venous phase shows almost complete venous filling; (F) late (recirculation) phase shows weaker fluorescence with staining of the optic disc

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  
  
  
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  The arterial phase starts about a second after the onset of choroidal fluorescence, and shows retinal arteriolar filling and the continuation of choroidal filling ( Fig. 14.19B ).

  
  
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  The arteriovenous (capillary) phase shows complete filling of the arteries and capillaries with early laminar flow in the veins in which the dye appears to line the venous wall leaving an axial hypofluorescent strip ( Fig. 14.19C ). This phenomenon reflects initial drainage from posterior pole capillaries filling the venous margins, as well as the small-vessel velocity profile, with faster plasma flow adjacent to vessel walls where cellular concentration is lower.

  
  
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  The venous phase. Laminar venous flow ( Fig. 14.19D ) progresses to complete filling ( Fig. 14.19E ), with late venous phase featuring reducing arterial fluorescence. Maximal perifoveal capillary filling is reached at around 20–25 seconds in patients with normal cardiovascular function, and the first pass of fluorescein circulation is generally completed by approximately 30 seconds.

  
  
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  The late (recirculation) phase demonstrates the effects of continuous recirculation, dilution and elimination of the dye. With each succeeding wave, the intensity of fluorescence becomes weaker although the disc shows staining ( Fig. 14.19F ). Fluorescein is absent from the retinal vasculature after about 10 minutes.

  
  
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  The dark appearance of the fovea ( Fig. 14.20A ) is caused by three factors ( Fig. 14.20B ):

  
  
  
  
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    Absence of blood vessels in the FAZ.

    
    
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    Blockage of background choroidal fluorescence due to the high density of xanthophyll at the fovea.

    
    
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    Blockage of background choroidal fluorescence by the RPE cells at the fovea, which are larger and contain more melanin and lipofuscin than elsewhere in the retina.

  
  

  
  

  
  

  

  
  

  
  

  (A) Dark appearance of the fovea on FA; (B) anatomical causative factors (see text)

  
  

Fluorescein access to the eye

Causes of hyperfluorescence

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  Autofluorescent compounds absorb blue light and emit yellow–green light in a similar fashion to fluorescein, but much more weakly. Autofluorescence can be detected on standard fundus photography with the excitation and barrier filters both in place; some modern digital cameras have enhanced autofluorescence detection capability, though imaging is most effective with scanning laser ophthalmoscopy. Autofluorescent lesions classically include optic nerve head drusen ( Fig. 14.21 ) and astrocytic hamartoma, but with increased availability of high-sensitivity imaging, patterns associated with a wide range of posterior segment pathology have been characterized.

  
  

  
  

  
  

  

  
  

  
  

  FAF imaging showing optic disc drusen

  
  
  
  
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  Pseudofluorescence (false fluorescence) refers to non-fluorescent reflected light visible prior to fluorescein injection; this passes through the filters due to the overlap of wavelengths passing through the excitation then the barrier filters. It is more evident when filters are wearing out.

  
  
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  Increased fluorescence may be caused by (a) enhanced visualization of normal fluorescein density, or (b) an increase in fluorescein content of tissues.

  
  
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  A window defect is caused by atrophy or absence of the RPE as in atrophic age-related macular degeneration ( Fig. 14.22A ), a full-thickness macular hole, RPE tears and some drusen. This results in unmasking of normal background choroidal fluorescence, characterized by very early hyperfluorescence that increases in intensity and then fades without changing size or shape ( Figs 14.22B and C ).

  
  

  
  

  
  

  

  
  

  
  

  Hyperfluorescence caused by window defects associated with dry age-related macular degeneration

  
  
  
  
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  Pooling in an anatomical space occurs due to breakdown of the outer blood–retinal barrier (RPE tight junctions):

  
  
  
  
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    In the subretinal space, e.g. CSR ( Fig. 14.23A ). This is characterized by early hyperfluorescence, which, as the responsible leak tends to be only small ( Fig. 14.23B ), slowly increases in intensity and area, the maximum extent remaining relatively well defined ( Fig. 14.23C ).

    
    

    
    

    
    

    

    
    

    
    

    Hyperfluorescence caused by pooling of dye in the subretinal space in central serous chorioretinopathy

    
    

    (Courtesy of S Chen – figs B and C)

    
    

    
    

    

    
    

    
    

    

    
    
    
    
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    In the sub-RPE space, as in pigment epithelial detachment (PED – Fig. 14.24A ). This is characterized by early hyperfluorescence ( Fig. 14.24B ) that increases in intensity but not in size ( Fig. 14.24C ).

    
    

    
    

    
    

    

    
    

    
    

    Hyperfluorescence caused by pooling of dye in the sub-retinal pigment epithelium (RPE) space in RPE detachment

    
    

  
  
  
  
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  Leakage of dye is characterized by fairly early hyperfluorescence, increasing with time in both area and intensity. It occurs as a result of breakdown of the inner blood–retinal barrier due to:

  
  
  
  
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    Dysfunction or loss of existing vascular endothelial tight junctions as in background diabetic retinopathy (DR), retinal vein occlusion (RVO), cystoid macular oedema (CMO – Fig. 14.25A ) and papilloedema.

    
    

    
    

    
    

    

    
    

    
    

    Causes of hyperfluorescence due to leakage. (A) Cystoid macular oedema; (B) proliferative diabetic retinopathy showing leakage from extensive vessels on the inferior macular arcade

    
    

    (Courtesy of P Gili – fig. A; S Chen – fig. B)

    
    

    
    

    

    
    
    
    
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    Primary absence of vascular endothelial tight junctions as in CNV, proliferative diabetic retinopathy ( Fig. 14.25B ), tumours and some vascular anomalies such as Coats disease.

  
  
  
  
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  Staining is a late phenomenon consisting of the prolonged retention of dye in entities such as drusen, fibrous tissue, exposed sclera and the normal optic disc (see Fig. 14.19F ), and is seen in the later phases of the angiogram, particularly after the dye has left the choroidal and retinal circulations.

Causes of hypofluorescence

Reduction or absence of fluorescence may be due to: (a) optical obstruction (masking or blockage) of normal fluorescein density ( Fig. 14.26 ) or (b) inadequate perfusion of tissue (filling defect).

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  Masking of retinal fluorescence. Preretinal lesions such as blood will block all fluorescence ( Fig. 14.27 ).

  
  

  
  

  
  

  

  
  

  
  

  Hypofluorescence – masking of all signal, including from retinal vessels, by preretinal haemorrhage (ILM = internal limiting membrane)

  
  
  
  
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  Masking of background choroidal fluorescence allows persistence of fluorescence from superficial retinal vessels:

  
  
  
  
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    Deeper retinal lesions, e.g. intraretinal haemorrhages, dense exudates.

    
    
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    Subretinal or sub-RPE lesions, e.g. blood ( Fig. 14.28 ).

    
    

    
    

    
    

    

    
    

    
    

    Hypofluorescence – blockage by sub- and intraretinal haemorrhage, showing persistence of signal from retinal vessels

    
    

    (Courtesy of S Chen)

    
    

    
    

    

    
    
    
    
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    Increased density of the RPE, e.g. congenital hypertrophy ( Fig. 14.29 ).

    
    

    
    

    
    

    

    
    

    
    

    Hypofluorescence caused by blockage of background fluorescence by congenital hypertrophy of the retinal pigment epithelium

    
    
    
    
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    Choroidal lesions, e.g. naevi.

  
  
  
  
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  Filling defects may result from:

  
  
  
  
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    Vascular occlusion, which may involve the retinal arteries, veins or capillaries (capillary drop-out – Fig. 14.30A ), or the choroidal circulation. FA is sometimes used to demonstrate optic nerve head filling defects as in anterior ischaemic optic neuropathy.

    
    

    
    

    
    

    

    
    

    
    

    Hypofluorescence caused by filling defects. (A) Capillary drop-out in diabetic retinopathy; (B) choroideremia

    
    

    (Courtesy of C Barry – fig. B)

    
    
    
    
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    Loss of the vascular bed as in myopic degeneration and choroideremia ( Fig. 14.30B ).

  
  

Causes of blocked fluorescence

Systematic approach to fluorescein angiogram analysis

A fluorescein angiogram should be interpreted methodically to optimize diagnostic accuracy.

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  Clinical findings, including the patient’s age and gender, should be noted before assessing the images.

  
  
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  Note whether images of right, left or both eyes have been taken.

  
  
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  Comment on any colour and red-free images and on any pre-injection demonstration of pseudo- or autofluorescence.

  
  
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  Looking at the post-injection images, indicate whether the overall timing of filling, especially arm-to-eye transit time, is normal.

  
  
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  Briefly scan through the sequence of images in time order for each eye in turn, initially concentrating on the eye with the greatest number of shots as this is likely to be the one about which there is greater concern. On the first review, look for any characteristic major diagnostic, especially pathognomonic, features; examples might include a lacy filling pattern or a ‘smokestack’ (see later).

  
  
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  Go through the run for each eye in greater detail, noting the evolution of any major features found on the first scan and then providing a description of any other findings using the methodical consideration of the causes of hyper- and hypofluorescence set out above.

Introduction

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  Advantages over FA. Whilst FA is an excellent method of studying the retinal circulation, it is of limited use in delineating the choroidal vasculature, due principally to masking by the RPE. In contrast, the near-infrared light utilized in indocyanine green angiography (ICGA) penetrates ocular pigments such as melanin and xanthophyll, as well as exudate and thin layers of subretinal blood, making this technique eminently suitable. An additional factor is that about 98% of ICG molecules bind to serum protein (mainly albumin), considerably higher than the binding of fluorescein; therefore, as choriocapillaris fenestrations are impermeable to larger protein molecules, most ICG is retained within choroidal vessels. Infrared light is also scattered less than visible light, making ICGA superior to FA in eyes with media opacity.

  
  
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  Image capture. ICG fluorescence is only 1/25th that of fluorescein so modern digital ICGA uses high-sensitivity videoangiographic image capture by means of an appropriately adapted camera. Both the excitation (805 nm) and emission (835 nm) filters are set at infrared wavelengths ( Fig. 14.31 ). Alternatively, scanning laser ophthalmoscopy (SLO) systems provide high contrast images, with less scattering of light and fast image acquisition rates facilitating high quality ICG video.

  
  

  
  

  
  

  

  
  

  
  

  Principles of indocyanine green angiography

  
  
  
  
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  The technique is similar to that of FA, but with an increased emphasis on the acquisition of later images (up to about 45 minutes) than with FA. A dose of 25–50 mg in 1–2 ml water for injection is used.

  
  
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  Phases of ICGA: (i) early – up to 60 seconds post-injection; (ii) early mid-phase – 1–3 minutes; (iii) late mid-phase – 3–15 minutes; and (iv) late phase – 15–45 minutes ( Fig. 14.32 ).

  
  

  
  

  
  

  

  
  

  
  

  Normal indocyanine green angiogram. (A) Early phase (up to 60 seconds post-injection) showing prominent choroidal arteries and poor early perfusion of the ‘choroidal watershed’ zone adjacent to the disc; (B) early mid-phase (1–3 minutes) showing greater prominence of choroidal veins as well as retinal vessels; (C) late mid-phase (3–15 minutes) showing fading of choroidal vessels but retinal vessels are still visible; diffuse tissue staining is also present; (D) late phase (15–45 minutes) showing hypofluorescent choroidal vessels and gradual fading of diffuse hyperfluorescence

  
  

  (Courtesy of S Milewski)

  
  

Adverse effects

ICGA is generally better tolerated than FA.

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  Nausea, vomiting and urticaria are uncommon, but anaphylaxis probably occurs with approximately equal incidence to FA.

  
  
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  Serious reactions are exceptionally rare. ICG contains iodide and so should not be given to patients allergic to iodine or possibly shellfish – iodine-free preparations such as infracyanine green are available.

  
  
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  ICGA is relatively contraindicated in liver disease (excretion is hepatic), and as with FA in patients with a history of a severe reaction to any allergen, moderate or severe asthma and significant cardiac disease. Its safety in pregnancy has not been established.

Diagnosis

Examples of pathological images are shown under the discussion of individual conditions where relevant.

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  Hyperfluorescence

  
  
  
  
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    A window defect similar to those seen with FA.

    
    
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    Leakage from retinal or choroidal vessels ( Fig. 14.33 ), the optic nerve head or the RPE; this gives rise to tissue staining or to pooling.

    
    

    
    

    
    

    

    
    

    
    

    ICGA image showing hyperfluorescence due to polyps and leakage in polypoidal choroidal vasculopathy

    
    

    (Courtesy of S Chen)

    
    
    
    
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    Abnormal retinal or choroidal vessels with an anomalous morphology (see Fig. 14.33 ) and/or exhibiting greater fluorescence than normal.

  
  
  
  
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  Hypofluorescence

  
  
  
  
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    Blockage (masking) of fluorescence. Pigment and blood are self-evident causes, but fibrosis, infiltrate, exudate and serous fluid also block fluorescence. A particular phenomenon to note is that in contrast to its FA appearance, a pigment epithelial detachment appears predominantly hypofluorescent on ICGA.

    
    
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    Filling defect due to obstruction or loss of choroidal or retinal circulation.

  
  

Indications

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  Polypoidal choroidal vasculopathy (PCV): ICGA is far superior to FA for the imaging of PCV (see Fig. 14.33 ).

  
  
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  Exudative age-related macular degeneration (AMD) . Conventional FA remains the primary method of assessment, but ICGA can be a useful adjunct, particularly if PCV is suspected.

  
  
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  Chronic central serous chorioretinopathy in which it is often difficult to interpret areas of leakage on FA. However, ICGA shows choroidal leakage and the presence of dilated choroidal vessels. Previously unidentified lesions elsewhere in the fundus are also frequently visible using ICGA.

  
  
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  Posterior uveitis. ICGA can provide useful information beyond that available from FA in relation to diagnosis and the extent of disease involvement.

  
  
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  Choroidal tumours may be imaged effectively but ICGA is inferior to clinical assessment for diagnosis.

  
  
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  Breaks in Bruch membrane such as lacquer cracks and angioid streaks are more effectively defined on ICGA than on FA.

  
  
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  If FA is contraindicated .

Introduction

Optical coherence tomography (OCT) is a non-invasive, non-contact imaging system providing high resolution cross-sectional images of the posterior segment. Imaging of the anterior segment (AS-OCT – Fig. 14.34A ) has also been increasingly adopted. OCT is analogous to B-scan ultrasonography but uses near-infrared light interferometry rather than sound waves, with images created by the analysis of interference between reflected reference waves and those reflected by tissue. Most instruments in current use employ spectral/Fourier domain technology, in which the mechanical movement required for image acquisition in older ‘time domain’ machines has been eliminated and the information for each point on the A-scan is collected simultaneously, speeding data collection and improving resolution. Promising newer modalities include swept-source (SS) OCT that can acquire images at a much higher rate and with extremely high retinal element resolution and better imaging depth; choroidal definition is improving rapidly. So-called adaptive optics allows correction of higher-order optical aberrations to greatly improve resolution, and wide-field, intraoperative, functional and Doppler (blood flow measurement) OCT applications may all have clinical utility in the future.

OCT imaging. (A) Anterior chamber angle; (B) spectral-domain image of the macula: ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner-segment/outer-segment junction; NFL = nerve fibre layer; ONL = outer nuclear layer; OPL = outer plexiform layer; RPE = retinal pigment epithelium

(Courtesy of J Fujimoto – fig. B)

Applications

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  Macula. The diagnosis and monitoring of macular pathology has been revolutionized by the advent of OCT imaging, e.g. AMD, diabetic maculopathy, macular hole, epiretinal membrane and vitreomacular traction, CSR and retinal venous occlusion.

  
  
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  Glaucoma. The widespread availability of OCT in ophthalmology suites for the assessment of medical retinal disease has contributed to its increased adoption as an adjunct to clinical and perimetric assessment in the management of glaucoma.

  
  
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  Retinal detachment. Distinction of retinal detachment from retinoschisis.

  
  
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  Anterior segment OCT has an expanding range of clinical applications such as suspected angle-closure glaucoma and corneal analysis (pachymetry, pre- and post-corneal refractive procedures, diagnosis and monitoring).

Normal appearance

High reflectivity structures can be depicted in a pseudo-colour image as red, intermediate as green-yellow and low reflectivity as blue-black. Fine retinal structures such as the external limiting membrane and ganglion cell layer can be defined ( Fig. 14.34B ). Detailed quantitative information on retinal thickness can be displayed numerically and in false-colour topographical maps; three-dimensional images can be constructed and different retinal layers studied in relief ( Fig. 14.35 ).

OCT printout showing cross-sectional views, retinal thickness measurement and different retinal layers in a three-dimensional reconstruction in a patient with a macular epiretinal membrane and consequent loss of the foveal depression