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Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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kanski 7th

characterized by very early hyperfluorescence which increases in intensity and then fades without changing size or shape (Fig. 14.24B and C).

4Pooling in an anatomical space occurs due to breakdown of the outer blood–retinal barrier (RPE tight junctions):

aIn the subretinal space as in central serous chorioretinopathy (Fig. 14.25A). This is characterized by early hyperfluorescence which, as the responsible leak tends to be only small, slowly increases in intensity and area, the maximum extent remaining relatively well-defined (Fig. 14.25B and C).

bIn the sub-RPE space as in pigment epithelial detachment (PED – Fig. 14.26A). This is characterized by early hyperfluorescence which increases in intensity but not in size (Fig. 14.26B and C).

5Leakage of dye is characterized by fairly early hyperfluorescence which increases in both area and intensity. It occurs as a result of breakdown of the inner blood–retinal barrier due to:

aDysfunction or loss of existing vascular endothelial tight junctions as in background diabetic retinopathy, retinal vein occlusion, cystoid macular oedema (Fig. 14.27A) and papilloedema.

bPrimary absence of vascular endothelial tight junctions as in choroidal neovascularization, proliferative diabetic retinopathy (Fig. 14.27B), tumours and some vascular anomalies such as Coats disease.

6Staining is a late phenomenon consisting of the prolonged retention of dye in tissue such as drusen, fibrous tissue, exposed sclera, and the normal optic disc (see Fig. 14.22E), and is seen in the later phases of the angiogram, particularly after the dye has left the choroidal and retinal circulations.

Fig. 14.24 Hyperfluorescence caused by a transmission (window) defect associated with dry age-related macular degeneration

Fig. 14.25 Hyperfluorescence caused by pooling of dye in the subretinal space in central serous chorioretinopathy

Fig. 14.26 Hyperfluorescence caused by pooling of dye in the sub-RPEspace in detachment of the RPE

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Fig. 14.27 Causes of hyperfluorescence due to leakage. (A) Proliferative diabetic retinopathy; (B) cystoid macular oedema

(Courtesy of P Gili – fig. B)

Causes of hypofluorescence

Reduction or absence of fluorescence may be due to: (a) optical obstruction (‘masking’ or blockage) of normal density of fluorescein in a tissue (Fig. 14.28) or (b) inadequate perfusion of tissue (‘filling defect’).

1Masking of retinal fluorescence. Pre-retinal lesions such as blood will block all fluorescence (Fig. 14.29). Deeper retinal lesions such as intraretinal haemorrhages and hard exudates will block only capillary fluorescence, sparing that from the larger retinal vessels.

2Masking of background choroidal fluorescence is caused by all conditions that block retinal fluorescence as well as those which block only choroidal fluorescence:

aSubretinal or sub-RPE lesions such as blood.

bIncreased density of the RPE that may be caused by congenital hypertrophy (Fig. 14.30).

cChoroidal lesions such as naevi.

3Filling defects may result from:

aVascular occlusion, which may involve the retinal arteries, veins or capillaries (‘capillary drop-out’ – Fig. 14.31A), or the choroidal circulation. FA is sometimes used to demonstrate optic nerve head filling defects as in anterior ischaemic optic neuropathy.

bLoss of the vascular bed as in myopic degeneration and choroideremia (Fig. 14.31B).

Fig. 14.28 Causes of blocked fluorescence

Fig. 14.29 Hypofluorescence caused by blockage of all fluorescence by a pre-retinal haemorrhage

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Fig. 14.30 Hypofluorescence caused by blockage of background fluorescence by congenital hypertrophy of the retinal pigment epithelium

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Fig. 14.31 Hypofluorescence caused by filling defects. (A) Capillary drop-out in diabetic retinopathy; (B) choroideremia

(Courtesy of C Barry – fig. B)

Systematic approach to reporting angiograms

A fluorescein angiogram should be interpreted methodically to optimize diagnostic accuracy. A suggested scheme: a Note the clinical findings, including the patient's age and gender, before assessing the angiogram.

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

cComment on any colour and red free images and on any pre-injection demonstration of pseudoor autofluorescence.

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

eBriefly 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/pathognomonic features; examples might include a lacy filling pattern or a smoke-stack (see later).

fGo 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 a methodical consideration of the causes of hyperand hypofluorescence set out above.

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Indocyanine green angiography

Principles

1Advantages over FA. Whilst FA is an excellent method of studying the retinal circulation, it is not helpful in delineating the choroidal vasculature, due principally to masking by the RPE. In contrast, the near-infrared light utilized in indocyanine green (ICG) angiography 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 advantage is that about 98% of ICG molecules bind to serum proteins (mainly albumin) on entering the circulation.

2Physiology. As the fenestrations of the choriocapillaris are impermeable to larger protein molecules, most ICG is retained within choroidal vessels, enhancing definition. Infrared light is also scattered less than visible light, making ICGA superior to FA in eyes with media opacities.

3Image capture. ICG fluorescence is only 1/25th that of fluorescein so modern digital ICGA uses high-sensitivity videoangiographic image capture by means of a modified camera with infrared excitation (805 nm) and emission (835 nm) filters (Fig. 14.32). 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.

4The technique is similar to that of FA, but with an increased emphasis on the acquisition of later images (up to about 45 minutes) than FA. A dose of 25–50 mg in 1–2 mL water for injection is used.

5The phases of a normal ICG angiogram are shown in Figure 14.33.

Fig. 14.32 Principles of indocyanine green angiography

(Redrawn from PG Watson, BL Hazelman, CE Pavésio and WR Green, from The Sclera and Systemic Disorders, Butterworth-Heinemann, 2004)

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Fig. 14.33 Normal indocyanine green angiogram. (A) Early phase (up to 60 seconds post-injection) shows prominent choroidal arteries and poor early perfusion of the ‘choroidal watershed’ zone; (B) early mid-phase (1–3 minutes) shows more prominence of choroidal veins as well as retinal vessels; (C) late mid-phase (3 –15 minutes) shows fading of choroidal vessels but retinal vessels are still visible; diffuse tissue staining is also present; (D) late phase (15–45 minutes) shows hypofluorescent choroidal vessels and gradual fading of diffuse hyperfluorescence

(Courtesy of S Milewski)

Adverse effects

ICGA is generally better tolerated than FA although the following problems may occur:

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

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

It is also 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. The safety of ICG in pregnancy has not been established.

Causes of hyperfluorescence

1A ‘window defect’ as in FA.

2Leakage from retinal or choroidal vessels, the optic nerve head or the RPE. This will give rise to tissue staining or to pooling.

3Abnormal retinal or choroidal vessels with an anomalous morphology and/or exhibiting greater fluorescence than normal.

Hypofluorescence

1Blockage (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.

2A ‘filling defect’ due to obstruction or loss of choroidal or retinal circulation.

Clinical indications

1Exudative age-related macular degeneration (AMD). Conventional FA remains the primary method of diagnosis and assessment, but ICGA is a useful adjunctive investigation.

2Polypoidal choroidal vasculopathy (PCV) in which ICGA is far superior to FA.

3Chronic 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.

4Posterior uveitis. ICGA can provide useful information beyond that available from FA in relation to diagnosis and to the extent of disease involvement.

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

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

7When FA is contraindicated.

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Optical coherence tomography

Definition

Optical coherence tomography (OCT) is a non-invasive, non-contact imaging system which provides high resolution cross-sectional images of the retina, vitreous and optic nerve head. Imaging of the anterior segment (AS-OCT) is also possible using the same technique although at present modified apparatus must be employed.

Principles

OCT is analogous to B-scan ultrasonography but uses near-infrared light interferometry rather than sound waves. Interferometry involves studying the pattern of interference created by the superposition of waves.

1Low (short) coherence light is used, in which interference occurs over only micrometers. The imaging beam is split into a sampling path directed onto the tissue being imaged, and a reference path reflected from a mirror, and an image is constructed by analyzing the intensity of reflected reference light in combination with the intensity of reflectivity of different target tissue structures. Tissue reflecting more light will create more intense interference. Scattered light is excluded from the image.

2In ‘time domain’ OCT, the position of the reference mirror is shifted towards and away from the source, essentially providing an axial scanning or A-scan function. Cross-sectional images are completed by scanning the sampling beam laterally across the target, yielding a two-dimensional data set usually displayed as a false-colour image.

3Newer OCT instruments utilize ‘spectral/Fourier domain’ analysis, in which mechanical movement has been eliminated and the information for each point on the A-scan is collected simultaneously, speeding image acquisition and improving resolution. Spectral OCT also permits the ready construction of three-dimensional images and the study in relief of different retinal layers.

Indications

1Diagnosis of cystoid macular oedema, macular holes, epiretinal membrane and vitreomacular traction, central serous chorioretinopathy, and to distinguish between long-standing retinal detachment and retinoschisis.

2Monitoring progression of disease processes and response to treatment e.g. AMD, diabetic macular oedema, preand postmacular hole surgery.

3Analysis of the optic nerve head and peripapillary retinal nerve fibre layer thickness, particularly in glaucoma diagnosis and monitoring.

4Anterior segment OCT has an expanding range of clinical applications such as imaging the anterior chamber angle in glaucoma, the cornea (pachymetry, preand post-corneal refractive procedures, disease diagnosis and monitoring) and the lens.

Normal appearance

High reflectivity structures are depicted as red, intermediate as green-yellow and low reflectivity as blue-black (Fig. 14.34). High resolution OCT (Fig. 14.34B) has the ability to identify fine retinal structures such as the external limiting membrane and ganglion cell layer which are not visualized as clearly with standard resolution (Fig. 14.34A). Detailed quantitative information on retinal thickness can be displayed numerically and in a false-colour topographical map (Fig. 14.35).

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Fig. 14.34 OCTdisplays. (A) Standard resolution of a normal macula in which most of the major retinal layers can be visualized; (B) high-resolution improves visualization of smaller structures such as the external limiting membrane (ELM) and ganglion cell layer (GCL); INL = inner nuclear layer; IPL = inner plexiformlayer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fibre layer; ONL = outer nuclear layer; OPL = outer plexiformlayer; RPE= retinal pigment epithelium

(Courtesy of J Fujimoto)

Fig. 14.35 Stratus OCTnumerical and false colour display of macular thickness in both eyes

(Courtesy of S Milewski)

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