Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Idiopathic Polypoidal

Choroidal Vasculopathy

Background Idiopathic polypoidal choroidal vasculopathy (IPCV) is sometimes described as a subtype of exudative ‘wet’ age-related macular degeneration (AMD).

Clinical features Originally described as presenting in hypertensive, black women aged 40–60 years with exudative retinal elevation, haemorrhagic pigment epithelial detachments (PEDs), and hard exudates. Appears to be common in East Asians and occurs in Caucasians, although the case definition is less certain. Unlike AMD, it often occurs beyond the arcades or near the optic disc. It may have a similar presentation to central serous retinopathy.

Investigations Indocyanine green (ICG) angiography shows characteristic collections of dilated choroidal vessels with terminal dilatations (polyps). These leak in the later frames (Fig. 10.34).

Treatment IPCV may resolve spontaneously (≈20%) but is often treated with focal laser to obliterate leaking dilatations (e.g. 200 mW, 200 micron spot size, 0.2 seconds), although the evidence for this is presently uncertain. It may not be possible to treat all lesions due to haemorrhage. Avoid laser to PEDs as this may cause an RPE tear.

Follow–up Six weeks after laser with repeat ICG.

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Idiopathic polypoidal choroidal vasculopathy

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Diabetic Retinopathy

Background Diabetics can lose vision from macular oedema, macular ischaemia, vitreous haemorrhage, and tractional retinal detachment. The ophthalmologist has several tasks: confirm the diagnosis; classify its severity and monitor accordingly; offer advice; apply retinal laser as required; and treat associated eye disease such as cataract.

Key studies

■Diabetic Retinopathy Study (DRS) : defined high-risk proliferative diabetic retinopathy (PDR, criteria below) and risk of severe visual loss with different levels of retinopathy. Established that panretinal photocoagulation (PRP) more than halves the risk of severe visual loss in high-risk PDR.

■Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) : population-based study showed that glycosylated haemoglobin levels and duration of diabetes are risk factors for progression of retinopathy.

■Early Treatment of Diabetic Retinopathy Study (ETDRS) : defined clinically significant macular oedema (criteria below) and showed that laser treatment approximately halves the risk of moderate visual loss.

■Diabetic Retinopathy Vitrectomy Study (DRVS) : demonstrated that early vitrectomy for vitreous haemorrhage (within 3 months) improved visual prognosis in type 1 diabetes.

■Diabetes Control and Complications Trial (DCCT) : demonstrated that intensive insulin treatment reduced the risk of sustained progression of retinopathy in type 1 diabetes when compared to conventional insulin treatment.

■United Kingdom Prospective Diabetes Study (UKPDS) : showed that tight blood pressure and glycaemic control in type 2 diabetes reduced retinopathy progression and visual loss.

Classification of retinopathy

■Mild non-proliferative diabetic retinopathy (NPDR) : At least one microaneurysm.

■Moderate non-proliferative diabetic retinopathy : intraretinal haemorrhages or microaneurysms < ETDRS standard photograph 2a (Fig. 10.35) and/or cotton-wool spots, venous beading, intraretinal microvascular abnormalities (IRMA).

■Severe nonproliferative diabetic retinopathy: relies on the

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1. Intraretinal haemorrhages or microaneurysms in four quadrants.

2.Venous beading ≥ ETDRS photograph 6a (Fig. 10.35) in two quadrants.

3.IRMA ≥ ETDRS photograph 8a (Fig. 10.35) in one quadrant.

■Very severe non-proliferative diabetic retinopathy: at least two of the criteria for severe NPDR.

■Non-high risk proliferative diabetic retinopathy : new vessels on the disc (NVD) or elsewhere (NVE), but criteria not met for high-risk proliferative diabetic retinopathy (PDR) below.

■High-risk proliferative diabetic retinopathy : at least one of the following:

1.NVD >1/3 disc area.

2. NVD plus vitreous or preretinal haemorrhage.

3. NVE >1/2 disc area plus preretinal or vitreous haemorrhage.

■Advanced proliferative diabetic retinopathy : tractional retinal detachment.

Macular exudates or thickening can occur with any severity of retinopathy. Treatment is advised if there is clinically significant macular oedema (CSMO) comprising at least one of the following:

■ Thickening of the retina within 500 μm of the fovea.

■Hard exudates located within 500 μm of the fovea with adjacent retinal thickening.

■Retinal thickening at least one disc area in size, part of which is located within one disc diameter of the fovea.

History Ask about the duration and type of diabetes, blood sugar control, smoking and associated disease, especially hypertension and renal disease. Identify the clinicians monitoring the patient’s diabetes.

Examination Examine the iris at high magnification for neovascularization (NVI). If present, or if IOP is elevated, perform gonioscopy to look for angle neovascularization (NVA). Perform careful fundus examination looking for atypical features. Exclude associated disease, especially posterior subcapsular cataracts. Classify severity.

Differential diagnosis

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Diabetic retinopathy

retinopathy; radiation retinopathy; leukaemia; anaemia; HIV microangiopathy.

■Proliferative diabetic retinopathy : vascular obstruction; sickle cell retinopathy; ocular ischaemic syndrome; sarcoidosis; Eales’ disease; tuberculosis; embolization from intravenous drug use.

Investigations Check blood pressure and fasting glucose if not diagnosed diabetic. Arrange fluorescein angiography if CSMO is present (to guide laser treatment) or if there is unexplained poor vision (to assess macular ischaemia). For interpretation of fluorescein angiograms, see page 415. Optical coherence tomography (OCT) may help confirm macular oedema.

Management Correspond with all relevant health workers to ensure glucose, blood pressure, and general health are well managed. Encourage smokers to stop and explain that poor glucose control threatens vision.

Ocular management depends on the findings:

■Nonproliferative diabetic retinopathy.

1. Absent or mild : refer to screening programme for annual review (1% risk of high-risk PDR in 1 year).

2. Moderate : review 6–9 monthly (4% risk of high-risk PDR in 1 year).

3. Severe : review 4–6 monthly (8% risk of high-risk PDR in 1 year).

4. Very severe : review 3–4 monthly (17% risk of high-risk PDR in 1 year).

■Proliferative retinopathy.

1. Non-high risk: review in 2 months (50% risk of high-risk PDR in 1 year). Consider PRP if poor attendance or poor diabetic control.

2. High-risk or iris new vessels : perform PRP within 1 week, preferably immediately. If there is coexisting CSMO, perform macular laser treatment first or at the same time. For laser technique, see page 433.

■Vitreous haemorrhage.

Treat mild vitreous haemorrhage as high-risk PDR. If the haemorrhage is dense enough to obscure the fundal view,

Apply PRP as haemorrhage clears and the view improves. Arrange vitreoretinal review if the haemorrhage persists for 1 month (type 1 diabetes), or 3–4 months (type 2)

(p. 534). Consider early referral if the other eye has poor accuity.

■Tractional retinal detachment.

If tractional retinal detachment threatens the macula, arrange vitreoretinal review (p. 534). If not, review 2–3 monthly depending on the retinopathy severity.

■Maculopathy.

1.Not clinically significant: review in 4–6 months.

2.Clinically significant macular oedema (criteria above): perform fluorescein angiography unless there is an isolated circinate, and treat as per ETDRS:

a.Focal laser to circinate ring.

b.Modified grid to areas of macular thickening.

c.Macular grid for diffuse thickening.

d. Avoid laser treatment to the edge of, or within, the foveal avascular zone (FAZ).

For laser settings and example treatments, see page 433. Consider earlier review for all categories if there is poor diabetic

or blood pressure control, or recent marked improvement in diabetic control (can transiently worsen retinopathy).

Diabetic retinopathy and cataract surgery

■Preoperative

1. Plan to operate early, before CSMO or high-risk PDR develop.

2. If possible, treat CSMO and wait until resolved before operating.

3. Treat high-risk PDR/NVI preoperatively if possible.

4. If there is no fundus view, perform B-scan ultrasound. If tractional retinal detachment or vitreous haemorrhage is present, refer for possible combined phaco-vitrectomy.

5. If there is high-risk PDR/NVI and it is not possible to complete preoperative PRP, perform intraoperative indirect PRP (allow extra time on the operating list).

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Diabetic retinopathy

advanced diabetic retinopathy or CSMO that cannot be treated preoperatively.

■ Intraoperative

1. Phacoemulsification technique is preferred.

2. Use a large-diameter optic, acrylic intraocular lens (to maximise retinal view postoperatively).

3. If intraoperative PRP is required, perform after crystalline lens removal and before intraocular lens insertion.

■ Postoperative

1.Macular oedema : examine the fundus within 1 week. If macular oedema is present it should be considered due to diabetes and treated as above. Macular oedema that develops after 1 week but before 6 months is probably pseudophakic and may resolve spontaneously. Manage expectantly for up to 1 year postoperatively.

2. Progression of retinopathy : increase frequency of review in eyes with severe NPDR or worse, as there is an increased risk of progression. Promptly treat high-risk PDR that occurs in the postoperative period.

Diabetic retinopathy and pregnancy

■Ideally, patients should be reviewed preconception to assess baseline retinopathy.

■Minimum review is at the end of the first trimester, weeks 20–24, then weeks 30–34.

■Arrange more frequent review if there is severe retinopathy/ maculopathy or poor diabetic control.

■Avoid fluorescein angiography if possible (p. 702).

■Treat by laser as required.

Central Retinal Vein Occlusion

Background Central retinal vein occlusion (CRVO) typically occurs in patients over 45 years secondary to retinal vein thrombosis. Risk factors include diabetes, hypertension, hyperlipidaemia, and glaucoma. CRVO in those aged less than 45 years may suggest a clotting disorder.

Clinical features CRVO produces painless visual loss in one eye. Signs include: retinal haemorrhages in four quadrants (Fig. 10.36); dilated tortuous retinal veins; optic disc swelling;

macular oedema; cotton-wool spots; neovascularization of the iris, angle, retina, or disc. Disc collateral vessels are a sign of resolution.

Classification

■Nonischaemic.

■Ischaemic.

1. Clinical examination : RAPD, VA <6/60, multiple cottonwool spots, dense midretinal haemorrhages, ‘blood and thunder fundus’.

2. Fluorescein angiogram : more than 10 disc areas of ischaemia.

History and examination Ask about glaucoma, systemic hypertension, raised lipids, diabetes or symptoms of diabetes (polyuria, polydipsia, weight loss). If younger than 45 years ask about thrombophilia: family history of thromboses aged <45 years; deep vein thrombosis; pulmonary emboli; thromboses in unusual sites, e.g. axillary vein; multiple miscarriages. Examine specifically for new vessels in the angle (undilated gonioscopy), iris, and optic nerve/retina. Examine both eyes for features of glaucoma. Perform digital ophthalmodynanometry to check for raised central retinal vein pressure. In normal eyes, the central retinal vein spontaneously pulses or can be made to ‘wink’ or collapse with minimal ocular pressure through the eyelids. In CRVO, the vein and artery ‘wink’ together or, in extreme cases, the artery is more easily compressed than the vein. The latter may also suggest reduced arterial pressure and ocular ischaemia, so compare with the fellow eye, assuming that is normal. Ocular ischaemia may present with loss of VA due to cilioretinal hypoperfusion.

Differential diagnosis Consider ocular ischaemic syndrome; diabetic retinopathy; optic disc swelling for other reasons; and radiation retinopathy.

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Central retinal vein occlusion

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Fig. 10.36: Central retinal vein occlusion.

Investigations Check BP, FBC, ESR, lipids (thyroid function if abnormal), plasma protein electrophoresis, and thrombophilia screen if suspicious. Arrange fluorescein angiogram if ischaemia is suspected (see Classification above). Diabetic work-up varies from random or fasting glucose, to HbA1c, glucose tolerance test, and diabetologist review. Normal fasting glucose is ≤6.0 mmol; impaired fasting glycaemia 6.1–6.9 mmol; ≥7.0 mmol suggests diabetes, but repeat if there are no diabetic symptoms.