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

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less well seen against a white background than a black letter. Contrast sensitivity represents a different aspect of visual function to that tested by the spatial resolution tests described above, which all use high-contrast optotypes.

•Many conditions reduce both contrast sensitivity and visual acuity, but under some circumstances (e.g. amblyopia, optic neuropathy, some cataracts, and higher order aberrations), visual function measured by contrast sensitivity can be reduced whilst VA is preserved.

•Hence, if patients with good VA complain of visual symptoms (typically evident in low illumination), contrast sensitivity testing may be a useful way of objectively demonstrating a functional deficit. Despite its advantages, it has not been widely adopted in clinical practice.

2The Pelli–Robson contrast sensitivity letter chart (Fig. 14.9) is viewed at 1 metre and consists of rows of letters of equal size (spatial frequency of 1 cycle per degree) but with decreasing contrast of 0.15 log units for groups of three letters. The patient reads down the rows of letters until the lowest-resolvable group of three is reached.

Fig. 14.9 Pelli–Robson contrast sensitivity letter chart

Amsler grid

The Amsler grid evaluates the 20° of the visual field centred on fixation (Fig. 14.10). It is principally useful in screening for and monitoring macular disease, but will also demonstrate central visual field defects originating elsewhere. Patients with a substantial risk of choroidal neovascularization should be provided with an Amsler recording chart for regular use at home.

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Fig. 14.10 Amsler grid superimposed on the macula

(Courtesy of A Franklin)

Charts

There are seven charts, each consisting of a 10 cm square (Figs 14.11 and 14.12).

Chart 1 consists of a white grid on a black background, the outer grid enclosing 400 smaller 5 mm squares. When viewed at about one-third of a metre, each small square subtends an angle of 1°.

Chart 2 is similar to chart 1 but has diagonal lines that aid fixation in patients unable to see the central spot as the result of a central scotoma.

Chart 3 is identical to chart 1 but has red squares. The red-on-black design aims to stimulate long wavelength foveal cones. It is used to detect subtle colour scotomas and desaturation that may occur in toxic maculopathies, optic neuropathies and chiasmal lesions.

Chart 4 consisting only of random dots is used mainly to distinguish scotomas from metamorphopsia, as there is no form to be distorted.

Chart 5 consists of horizontal lines and is designed to detect metamorphopsia along specific meridians. It is of particular value in the evaluation of patients describing difficult reading.

Chart 6 is similar to chart 5 but has a white background and the central lines are closer together enabling more detailed evaluation. Chart 7 exhibits a fine central grid, each square subtending an angle of a half degree, and is therefore more sensitive.

Fig. 14.11 Amsler grid chart

(Courtesy of A Franklin)

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Fig. 14.12 Amsler charts 2–7

(Courtesy of A Franklin)

Technique

The pupils should not yet have been dilated, and in order to avoid a photostress effect the eyes should not yet have been examined on the slit-lamp. A presbyopia correction should be worn if appropriate. The chart should be well illuminated and held at a comfortable reading distance. One eye is covered.

aThe patient is asked to look directly at the central dot with the uncovered eye, to keep looking at this, and to report any distortion or waviness of the lines.

bReminding the patient to maintain fixation on the central dot, ask if there are blurred areas or blank spots anywhere on the grid. Patients with macular disease often report that the lines are wavy whereas those with optic neuropathy often remark that some of the lines are missing or faint but not distorted.

cThe patient is asked if he can see all four corners and all four sides of the square – a missing corner or border should raise the possibility of causes other than macular disease such as glaucomatous field defects or retinitis pigmentosa.

d The patient is given a recording sheet and pen and asked to draw any anomalies on a recording chart (Fig. 14.13).

eThe other eye is tested.

Fig. 14.13 Amsler recording sheet shows wavy lines indicating metamorphopsia and a dense scotoma

In clinical practice, testing is very commonly carried out simply using the recording chart, upon which patients can then illustrate any

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abnormality directly.

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fundus Fluorescein angiography

Principles

1Fluorescence 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) and represents the maximal absorption of light energy by fluorescein. Molecules stimulated by this wavelength will be excited to a higher energy level and will emit light of about 530 nm (yellow-green; Fig. 14.14).

2Fluorescein (sodium fluorescein) is an orange water-soluble dye that, when injected intravenously, remains largely intravascular and circulates in the blood stream. It undergoes both renal and hepatic metabolism and is excreted in the urine over 24–48 hours.

3Fluorescein angiography (FA) involves photographic surveillance of the passage of fluorescein through the retinal and choroidal circulations following intravenous injection (Fig. 14.15).

4Fluorescein binding. On intravenous injection, 70–85% of fluorescein molecules bind to serum proteins, the residue remaining unbound.

5Outer blood–retinal barrier. The major choroidal vessels are impermeable to both bound and free fluorescein. However, the walls of the choriocapillaris contain multiple fenestrations through which free fluorescein molecules escape into the extravascular space. They then pass across Bruch membrane but on reaching the retinal pigment epithelium (RPE) are blocked by intercellular complexes termed tight junctions or zonula occludentes (Fig. 14.16).

6Inner blood–retinal barrier is composed principally of the tight junctions between retinal capillary endothelial cells, across which neither bound nor free fluorescein can pass (Fig. 14.17A); the basement membrane and pericytes play only a minor role in this regard. Disruption of the inner blood–retinal barrier will permit leakage of both bound and free fluorescein into the extravascular space (Fig. 14.17B).

7Filters of two types are used to ensure that blue light enters the eye and only yellow-green light enters the camera (Fig. 14.18).

aA cobalt blue excitation filter through which passes white light from the camera. The emerging blue light enters the eye and excites the fluorescein molecules in the retinal and choroidal circulations, which then emit light of a longer wavelength (yellow-green).

bA yellow-green barrier filter then blocks any reflected blue light from the eye, allowing only the emitted yellow-green fluorescent light to pass through.

8Image capture in modern devices tends to be via the charge-coupled device (CCD) of a digital camera, with older cameras using fast black-and-white film. Digital image capture permits immediate picture availability, easy storage and access, image manipulation and enhancement.

Fig. 14.14 Excitation and emission of fluorescein

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Fig. 14.15 Injection of fluorescein into the antecubital vein and its passage into the eye

Fig. 14.16 The outer blood–retinal barrier (ZO= zonula occludentes; BM= Bruch membrane)

Fig. 14.17 Inner blood–retinal barrier. (A) Intact; (B) disrupted (E= endothelial cell; B.M. = basement membrane; P= pericyte)

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Fig. 14.18 Principles of fluorescein angiography

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

It must be emphasized that FA should only be performed if the findings are likely to influence management.

Technique

1Preliminaries. A good quality angiogram requires adequate pupillary dilatation and clear media. The patient is asked about contraindications to FA.

•Fluorescein allergy is an absolute contraindication, and a history of a severe reaction to any allergen is a strong relative contraindication.

•Other relative contraindications include renal failure (lower the fluorescein dose if angiography is necessary), pregnancy, moderate-severe asthma and significant cardiac disease.

•It should be noted that allergy to iodine and seafood allergies are not contraindications to FA – fluorescein contains no iodine – but are absolute contraindications to indocyanine green (ICG) angiography as ICG contains iodine.

•Facilities and arrangements must be in place to address possible adverse events. This includes adequate staffing, resuscitation trolley, drugs for treatment of anaphylaxis, couch (or reclining chair) and a receiver in case of vomiting.

•The procedure is explained and formal consent taken. It is important to mention the common and serious adverse effects (Table 14.2), particularly the invariable skin and urine staining and the very common occurrence of nausea immediately following fluorescein injection.

2Technique

aThe patient is seated comfortably in front of the fundus camera, and an intravenous cannula inserted. A standard venous cannula should be used 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.

bFluorescein, usually 5 mL of a 10% solution, is drawn up into a syringe. In eyes with opaque media, 3 mL of a 25% solution may afford better results.

c If not already obtained, colour photographs are taken.

dA ‘red-free’ image is captured (Table 14.3).

eIf indicated, a pre-injection study is performed to detect autofluorescence (see below), with both the excitation and barrier filters in place.

fFluorescein is injected over the course of a few seconds.

gImages are taken at approximately 1 second intervals, beginning 5–10 seconds after injection and continuing through the desired phases.

hIf the pathology is monocular, control pictures of the opposite eye should still be taken, usually after the transit phase has been photographed in one eye.

iIf appropriate, late photographs may be taken after 10 minutes to show leakage, and occasionally after 20 minutes.

jStereo 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; such images are actually pseudostereo, true stereo requiring simultaneous pictures from differing angles.

Table 14.2 -- Adverse events in fluorescein angiography

•Discolouration of skin and urine (invariable)

•Extravasation of injected dye (painful local reaction)

•Nausea very common, vomiting relatively uncommon

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•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)

Table 14.3 -- Red-free fundus photography

•Image captured prior to fluorescein injection

•Taken with the yellow-green barrier filter in place, blocking red light

•Red structures appear black, heightening contrast

•Vasculature and haemorrhages easy to identify

•Visibility of retinal nerve fibre layer defects and other retinal details enhanced

Phases of the angiogram

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. Because the route to the retinal circulation is slightly longer than that to the choroidal, the latter is filled about 1 second before the former (Fig. 14.19). In the choroidal circulation, precise details are often not discernible, mainly because of rapid leakage of free fluorescein from the choriocapillaris and also because the melanin in the RPE cells blocks choroidal fluorescence. The angiogram consists of the following overlapping phases (Fig. 14.20).

1The 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. 14.21).

2The arterial phase starts about a second after the onset of choroidal fluorescence, and shows retinal arteriolar filling and the continuation of choroidal filling (Fig. 14.22A).

3The 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. 14.22B). 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.

4The venous phase. Laminar venous flow (Fig. 14.22C) progresses to complete filling (Fig. 14.22D), 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.

5The 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. 14.22E). Fluorescein is absent from the retinal vasculature after about 10 minutes.

6The dark appearance of the fovea (Fig. 14.23A) is caused by three factors (Fig. 14.23B):

•Absence of blood vessels in the FAZ.

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

•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.

Fig. 14.19 Entry of fluorescein into the choroidal and retinal circulations

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Fig. 14.20 Four phases of the fluorescein angiogram

Fig. 14.21 Choroidal phase shows patchy choroidal filling as well as filling of a cilioretinal artery

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Fig. 14.22 Normal fluorescein angiogram. (A) Arterial phase shows filling of the choroid and retinal arteries; (B) arteriovenous (capillary) phase shows complete arterial filling and early laminar venous flow; (C) early venous phase shows marked laminar venous flow; (D) mid-venous phase shows almost complete venous filling; (E) late (elimination) phase shows weak fluorescence with staining of the optic disc

Fig. 14.23 Reasons for the dark appearance of the fovea

Causes of hyperfluorescence

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

1Autofluorescence compounds absorb blue light and emit yellow-green light in a similar fashion to fluorescein. It is imaged much more effectively by scanning laser ophthalmoscopy but can also be detected on standard fundus photography in exposed optic nerve head drusen (see Fig. 19.24B) and sometimes with lipofuscin in retinal drusen and other abnormalities such as astrocytic hamartoma (see Fig. 12.42D) and angioid streaks.

2Pseudofluorescence (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.

3A ‘window defect’ is caused by atrophy or absence of the RPE (Fig. 14.24A) as in atrophic age-related macular degeneration, fullthickness macular holes, RPE tears and some drusen. This results in unmasking of normal background choroidal fluorescence,

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