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

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Fig. 13.14 Intraretinal microvascular abnormalities. (A) Histology shows arteriolar-venular shunt and a few microaneurysms within a poorly perfused capillary bed – flat preparation of Indian ink-injected retina; phase contrast microscopy; (B) clinical appearance

(Courtesy of J Harry – fig. A; Moorfields Eye Hospital – fig. B)

Arterial changes

Subtle retinal arteriolar dilatation may be an early marker of ischaemic dysfunction. When significant ischaemia is present these include peripheral narrowing, silver-wiring and obliteration (Fig. 13.15), similar to the late appearance following a branch retinal artery occlusion.

Fig. 13.15 Peripheral arteriolar occlusion

Proliferative retinopathy

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It has been estimated that over one-quarter of the retina must be non-perfused before PDR develops. Although preretinal new vessels may arise anywhere in the retina, they are most commonly seen at the posterior pole. Fibrous tissue, initially fine, gradually develops in association as vessels increase in size.

1New vessels at the disc (NVD) describes neovascularization on or within one disc diameter of the optic nerve head (Fig. 13.16A –C).

2New vessels elsewhere (NVE) describes neovascularization further away from the disc (Fig. 13.17A and B) that may be associated with fibrosis (Fig. 13.17D) if long-standing.

3New vessels on the iris (NVI), also known as rubeosis iridis, carry a high likelihood of progression to neovascular glaucoma.

4FA, although not required to make the diagnosis, highlights neovascularization during the early phases of the angiogram (see Fig. 13.16D) and shows hyperfluorescence during the later stages due to intense leakage of dye from neovascular tissue (Fig. 13.17D).

Fig. 13.16 Disc new vessels. (A) Mild; (B) severe; (C) very severe; (D) FA early phase highlights the vessels

(Courtesy of P Gili)

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Fig. 13.17 New vessels elsewhere. (A) Mild; (B) severe; (C) associated with fibrosis; (D) FA late phase shows capillary non-perfusion and hyperfluorescence due to leakage

(Courtesy of C Barry – fig. D)

Treatment

Argon laser treatment of clinically significant macular oedema

1Indications

•All eyes with CSMO should be considered for laser photocoagulation irrespective of the level of visual acuity, because treatment reduces the risk of visual loss by 50%. However, options should always be discussed with the patient, and if visual acuity is good some authorities prefer to recommend careful observation, as macular laser is not without risk, and oedema sometimes resolves spontaneously.

•Pre-treatment FA is useful to delineate the area and extent of leakage, and to detect ischaemic maculopathy (see Fig. 13.10) which carries a poor prognosis and if severe is a relative contraindication to treatment.

2Focal treatment (Fig. 13.18A)

•Burns are applied to microaneurysms and microvascular lesions in the centre of rings of exudates located 500–3000 µm from the centre of the macula.

•The spot size is 50–100 µm and exposure time 0.1 second with sufficient power to obtain gentle whitening or darkening of the microaneurysm.

•Treatment of lesions up to 300 µm from the centre of the macula may be considered if CSMO persists despite previous treatment and visual acuity is less than 6/12. In these cases a shorter exposure time of 0.05 second is recommended.

3Grid treatment (Fig. 13.18B)

•Burns are applied to areas of diffuse retinal thickening more than 500 µm from the centre of the macula and 500 µm from the temporal margin of the optic disc.

•The spot size is 100 µm and exposure time 0.1 second giving a very light intensity burn.

•Treatment should be lighter if significant macular ischaemia is present.

4Results. Approximately 70% of eyes achieve stable visual acuity, 15% show improvement and 15% subsequently deteriorate. Since it may take up to 4 months for the oedema to resolve, re-treatment should not be considered prematurely.

5Poor prognostic factors

aOcular factors include significant macular ischaemia, exudates involving the fovea, diffuse macular oedema, CMO and severe retinopathy at presentation.

bSystemic factors include uncontrolled hypertension, renal disease, poorly-controlled blood glucose (elevated HbA1c levels).

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Fig. 13.18 Laser photocoagulation for clinically significant macular oedema. (A) Appearance several weeks following focal laser photocoagulation shows laser scars and absence of hard exudates; (B) appearance immediately following grid laser photocoagulation

Other treatments for maculopathy

Argon laser remains the primary therapeutic modality, but numerous other forms of treatment have shown promising results.

1Other lasers

aFrequency-doubled Nd:YAG laser offers the potential of a less destructive retinal effect than argon, in which the energy employed is the lowest capable of producing barely visible burns at the level of the RPE. The ‘Pattern Scan Laser’ (Pascal) uses frequency-doubled micropulse YAG in single shot mode or in a predetermined array of up to 56 shots applied in less than a second. This greatly improves patient comfort as compared with conventional argon laser.

bMicropulse diode laser in which short duration (microseconds) burns are applied to the RPE without significantly affecting the outer retina and choriocapillaris.

2Intravitreal anti-vascular endothelial growth factor (anti-VEGF) agents. A large multicentre trial (The Diabetic Retinopathy Research Network Laser-Ranibizumab-Triamcinolone Study) recently showed that intravitreal injection of 0.5 mg ranibizumab, initially given monthly for 3 months, with prompt or deferred (≥24 weeks) macular laser had significantly superior visual and OCT outcomes to laser alone in eyes with diabetic macular oedema involving the fovea. It is likely that intravitreal VEGF inhibitors will play an increasingly prominent role in the treatment of diabetic retinopathy.

3Intravitreal triamcinolone. The study described above also investigated the effect of intravitreal triamcinolone injection, finding that in pseudophakic eyes steroid injection followed by prompt laser may be as effective as ranibizumab at improving vision and reducing retinal thickening. However, there was a significant risk of an elevation of intraocular pressure. No corresponding visual benefit above laser was shown for phakic eyes, which also had a substantially increased rate of cataract surgery by 2 years.

4Pars plana vitrectomy may be indicated when macular oedema is associated with tangential traction from a thickened and taut posterior hyaloid. It has also been suggested that some eyes without a taut posterior hyaloid may benefit from vitrectomy. Clinically, a taut thickened posterior hyaloid is characterized by an increased glistening of the pre-macular vitreous face. FA typically shows diffuse leakage and prominent CMO, but OCT is usually the definitive assessment.

5Lipid-lowering drugs may reduce the requirement for laser treatment, and studies are ongoing.

Laser photocoagulation for proliferative retinopathy

The Diabetic Retinopathy Study (DRS) established the characteristics of high-risk proliferative disease and investigated the effect of panretinal photocoagulation (PRP). The benefits demonstrated included:

•Mild NVD with haemorrhage carries a 26% risk of visual loss, which is reduced to 4% with treatment.

•Severe NVD without haemorrhage carries a 26% risk of visual loss, which is reduced to 9% with treatment.

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•Severe NVD with haemorrhage carries a 37% risk of visual loss, which is reduced to 20% with treatment.

•Severe NVE with haemorrhage carries a 30% risk of visual loss, which is reduced to 7% with treatment.

1Indications. Laser therapy is aimed at inducing the involution of new vessels and thereby preventing visual loss; see Table 13.1 for specific indications. It should be noted that:

•PRP influences only the vascular component of the fibrovascular process. Eyes in which new vessels have regressed leaving only fibrous tissue should not be re-treated.

•If CSMO is also present, laser for this should preferably be carried out prior to PRP or at the same session; the intensity and amount of PRP should be kept to the lowest level likely to be effective, and may be spread over multiple sessions; adjunctive intravitreal steroid or an anti-VEGF agent may improve the outcome in this situation.

2Informed consent. Patients should be advised that PRP may occasionally cause visual field defects of sufficient severity to legally preclude driving a motor vehicle; they should also be made aware that there is some risk to central vision, and that night and colour vision may be affected.

3Laser settings

aSpot size depends on the contact lens used. With the Goldmann lens spot size is set at 200–500 µm, but with a panfundoscopic-type lens it is set at 100–300 µm because of induced magnification (varies with exact lens used). The main effect is related to surface area of retina treated rather than the number of burns; a small variation in the size of the laser burn therefore has a pronounced effect on area treated (area = πr2). In the beginner's hands, a panfundoscopic lens is perhaps safer than the Goldmann, as it is more difficult to inadvertently photocoagulate the posterior pole through the former.

bDuration of the burn is 0.05–0.1 second.

cPower should be sufficient to produce only a light intensity burn (Fig. 13.19A), with the intention of stimulating the retinal pigment epithelium rather than ablating the retina (Fig. 13.19B).

4Initial treatment involves 1500–2000 burns in a scatter pattern extending from the posterior fundus to cover the peripheral retina in one or more sessions; PRP completed in a single session carries a slightly higher risk of complications. The amount of treatment it is possible to apply during one session is governed by the patient's pain threshold; discomfort tends to be least at the posterior pole and greatest in the periphery and over the horizontal neurovascular bundle, and tends to worsen with successive sessions. Topical anaesthesia is adequate in most patients, although peribulbar or sub-Tenon anaesthesia may be necessary. A suggested treatment sequence is as follows:

aStep 1. Close to the disc (Fig. 13.20A); below the inferior temporal arcades (Fig. 13.20B and C).

bStep 2. Protective barrier around the macula (Fig. 13.21A) to prevent inadvertent treatment of the fovea; above the superotemporal arcade (Fig. 13.21B and C). If necessary, the retina just inside the arcades can be treated.

cStep 3. Nasal to the disc (Fig. 13.22A and B); completion of posterior pole treatment (Fig. 13.22C). Many practitioners leave two disc diameters untreated at the nasal side of the disc, to preserve paracentral field.

dStep 4. Peripheral treatment (Fig. 13.23A and B) until completion (Fig. 13.23C).

In very severe PDR it is advisable to treat the inferior fundus first, since any vitreous haemorrhage will gravitate inferiorly and obscure this area, precluding further treatment.

5Follow-up is after 4–6 weeks. In eyes with severe NVD, 3000 or more burns may be required. Occasionally complete elimination of NVD may be difficult but once the tips of the vessels start to undergo fibrosis they pose much less of a threat to vision.

6Signs of involution consist of regression of neovascularization leaving ‘ghost’ vessels or fibrous tissue (Fig. 13.24), decrease in venous changes, absorption of retinal haemorrhages and disc pallor. In most eyes, once the retinopathy is quiescent, stable vision is maintained. In a few eyes, recurrences occur despite an initial satisfactory response, and patients should remain under observation.

7Treatment of recurrences may involve further laser photocoagulation filling in any gaps between previous laser scars or utilizing indirect laser to treat very peripheral retina.

8Fibrosis associated with neovascularization (see Fig. 13.17C) is important, since significant fibrous proliferation, although less likely to bleed carries an increased risk of tractional retinal detachment.

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Fig. 13.19 (A) Appropriate laser burns; (B) appearance several weeks after completion of treatment

(Courtesy of C Barry – fig. B)

Fig. 13.20 PRPtechnique – step 1

Fig. 13.21 PRPtechnique – step 2

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Fig. 13.22 PRPtechnique – step 3

Fig. 13.23 PRPtechnique – step 4

Fig. 13.24 Treatment of proliferative diabetic retinopathy. (A) Severe proliferative disease; (B) 3 months later new vessels have regressed and there is residual fibrosis at the disc

(Courtesy of S Milewski)

VEGF inhibition for proliferative retinopathy

Intravitreal anti-VEGF injection is likely to have an increasing role in the treatment of PDR, probably as an adjunct to laser. A particular indication may be to encourage the resolution of persistent vitreous haemorrhage, avoiding vitrectomy in some patients.

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Advanced diabetic eye disease

Advanced diabetic eye disease is a serious vision-threatening complication of DR that occurs in patients in whom treatment has been inadequate or unsuccessful. Occasionally, advanced disease is evident at, or prompts, presentation.

Diagnosis

1Haemorrhage may be preretinal (retrohyaloid, Fig. 13.25A), intragel (Fig. 13.25B) or both. Intragel haemorrhages usually take longer to clear than preretinal haemorrhages because the former are usually the result of a more extensive bleed. In some eyes, altered blood becomes compacted on the posterior vitreous face to form an ‘ochre membrane’. Patients should be warned that bleeding may be precipitated by severe physical exertion or straining, hypoglycaemia and direct ocular trauma. Ultrasonography is used in eyes with dense vitreous haemorrhage to detect the possibility of associated retinal detachment (see Fig. 17.1D).

2Tractional retinal detachment (Fig. 13.25C) is caused by progressive contraction of fibrovascular membranes over areas of vitreoretinal attachment. Posterior vitreous detachment in eyes with PDR is often incomplete due to the strong adhesions between cortical vitreous and areas of fibrovascular proliferation (see Ch. 16).

3Tractional retinoschisis with or without retinal detachment may also occur.

4Rubeosis iridis (iris neovascularization – Fig. 13.25D) may occur in eyes with PDR, and if severe may lead to neovascular glaucoma. Rubeosis is particularly common in eyes with severe retinal ischaemia or persistent retinal detachment following unsuccessful pars plana vitrectomy.

Fig. 13.25 Advanced diabetic eye disease. (A) Retrohyaloid haemorrhage; (B) intragel haemorrhage; (C) tractional retinal detachment; (D) rubeosis iridis

(Courtesy of C Barry – figs A and D)

Indications for pars plana vitrectomy

1Severe persistent vitreous haemorrhage that precludes adequate PRP is the most common indication. In the absence of rubeosis iridis, vitrectomy has traditionally been considered within 3 months of the initial vitreous haemorrhage in type 1 diabetics and in most cases of bilateral haemorrhage. However, the availability of intravitreal anti-VEGF injections may modify this approach.

2Progressive tractional RD threatening or involving the macula must be treated without delay (Fig. 13.26A). However, extramacular tractional detachments may be observed, since they often remain stationary for prolonged periods.

3Combined tractional and rhegmatogenous RD should be treated urgently, even if the macula is not involved, because subretinal fluid is likely to spread quickly to involve the macula.

4Premacular subhyaloid haemorrhage, if dense (Fig. 13.26B) and persistent should be considered for vitrectomy because, if untreated, the internal limiting membrane or posterior hyaloid face may serve as a scaffold for subsequent fibrovascular proliferation and consequent tractional macular detachment or macular epiretinal membrane formation. Some cases of successful dispersion with YAG lazer (hyaloidotomy) have been reported.

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Fig. 13.26 Indications for pars plana vitrectomy. (A) Tractional detachment involving the macula; (B) large premacular subhyaloid haemorrhage

Visual results of pars plana vitrectomy

Visual results depend on the specific indications for surgery and the complexity of pre-existing vitreoretinal abnormalities. In general, about 70% of cases achieve visual improvement, about 10% are made worse and the rest are unchanged. It appears that the first few postoperative months are vital. If an eye is doing well after 6 months, then the long-term outlook is good because the incidence of subsequent visionthreatening complications is low. Favourable prognostic factors include:

•Good preoperative visual function.

•Age 40 years or less.

•Absence of preoperative rubeosis and glaucoma.

•Previous PRP to at least one-quarter of the fundus.

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Retinal venous occlusive disease

Pathogenesis

Arteriolosclerosis is an important causative factor for branch retinal vein occlusion (BRVO). Because a retinal arteriole and its corresponding vein share a common adventitial sheath, thickening of the arteriole appears to compress the vein. This causes secondary changes, including venous endothelial cell loss, thrombus formation and potential occlusion. Similarly, the central retinal vein and artery share a common adventitial sheath at arteriovenous crossings posterior to the lamina cribrosa so that atherosclerotic changes of the artery may compress the vein and precipitate central retinal vein occlusion (CRVO). It therefore appears that both arterial and venous disease contribute to retinal vein occlusion. Venous occlusion causes elevation of venous and capillary pressure with stagnation of blood flow. Stagnation results in hypoxia of the retina drained by the obstructed vein, which, in turn, results in damage to the capillary endothelial cells and extravasation of blood constituents. The tissue pressure is increased, causing further stagnation of the circulation and hypoxia, so that a vicious cycle is established.

Predisposing factors

Common

1Age is the most important factor; over 50% of cases occur in patients over the age of 65 years.

2Hypertension is present in up to 73% of RVO patients over the age of 50 years and in 25% of younger patients. It is most prevalent in patients with BRVO, particularly when the site of obstruction is at an arteriovenous crossing. Inadequate control of hypertension may also predispose to recurrence of RVO in the same or fellow eye.

3Hyperlipidaemia (total cholesterol >6.5 mmol/l) is present in 35% of patients, irrespective of age.

4Diabetes mellitus is present in about 10% of cases over the age of 50 years but is uncommon in younger patients. This may be due to an associated higher prevalence of other cardiovascular risk factors such as hypertension which is present in 70% of type 2 diabetics.

5Oral contraceptive pill. In younger females the contraceptive pill is the most common underlying association, and should not be taken following retinal vein occlusion. The risk may be exacerbated by thrombophilia.

6Raised intraocular pressure increases the risk of CRVO, particularly when the site of obstruction is at the edge of the optic cup.

7Smoking. Current smoking may be associated with an increased incidence of RVO, though studies have shown inconsistent results.

Uncommon

Uncommon predispositions (listed below) may assume more importance in patients under the age of 50 years.

1Myeloproliferative disorders

•Polycythaemia.

•Abnormal plasma proteins (e.g. myeloma, Waldenström macroglobulinaemia).

2Acquired hypercoagulable states

•Hyperhomocysteinaemia.

•Lupus anticoagulant and antiphospholipid antibodies.

•Dysfibrinogenaemia.

3Inherited hypercoagulable states

•Activated protein C resistance (factor V Leiden mutation).

•Protein C deficiency.

•Protein S deficiency.

•Antithrombin deficiency.

•Prothrombin gene mutation.

•Factor Xll deficiency.

4Inflammatory disease associated with occlusive periphlebitis

•Behçet syndrome.

•Sarcoidosis.

•Wegener granulomatosis.

•Goodpasture syndrome.

5Miscellaneous

•Chronic renal failure.

•Causes of secondary hypertension (e.g. Cushing syndrome) or hyperlipidaemia (e.g. hypothyroidism).

•Orbital disease.

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