Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Diabetic vitreoretinal surgery

Diabetic Vitreoretinal Surgery

Persistent vitreous haemorrhage

Background The fragile new vessels that define proliferative diabetic retinopathy may bleed into the vitreous cavity, reducing VA, and preventing treatment with panretinal photocoagulation (PRP). As 20% of haemorrhages clear within 1 year, surgical timing is crucial: operate early and expose some patients to unnecessary surgical risks; operate late and delay PRP and visual recovery.

Key study Diabetic Retinopathy Vitrectomy Study1 For type 1 diabetics, early vitrectomy (1–6 versus 12 months) increased the chance of VA ≥6/12 at 2 years. Not significant for type 2, but none had intraoperative PRP and 30% had lensectomy. Surgical technique has improved.

History Determine age, if type 1 or 2 diabetes, duration of visual loss, total number of PRP burns and surgical risk factors.

Examination Note VA, IOP, rubeosis, lens status, RAPD, density of vitreous haemorrhage, retinopathy and fellow eye disease.

Investigations Arrange ultrasound to show vitreous or retinal detachment. Repeat every 2 months if the fundal view remains inadequate.

Treatment Vitrectomy timing:

■Type 1 diabetics at 3 months.

■Type 2 at 4–6 months.

Consider earlier surgery if rubeosis, raised IOP, incomplete PRP, or poor fellow eye VA. Simultaneous vitrectomy and cataract surgery is often required but avoid cataract surgery if possible, as diabetics may get posterior synechiae from increased post operative inflammation after combined surgery.

Consent

■Benefit : improve and stabilize vision. VA ≥6/12 in 36% of type 1 diabetics, 16% of type 2 diabetics.1

■Risk : rapid visual loss including NPL. Haemorrhage may recur but resolves more quickly in vitrectomized eyes. See Risks of vitrectomy (p. 532) and PRP (p. 434).

Recurrent vitreous haemorrhage

May occur despite adequate PRP, if inactive new vessels have ongoing vitreous traction. Vitrectomy can relieve vascular traction if haemorrhages are frequent and slow to clear.

Tractional retinal detachment

Background Proliferative fibrovascular membranes may cause tractional retinal detachments. Consider surgery if they involve or threaten the fovea.

Examination Note VA, IOP, rubeosis, RAPD, lens status, presence of posterior vitreous detachment, extent of PRP and membranes, retinal breaks, and fellow eye disease.

Treatment Vitrectomy and membrane removal by delamination (horizontal dissection between the membrane and retina), segmentation (vertical membrane division to relieve tangential traction), or en bloc. PRP is often required.

Consent

■Benefit : improve or stabilize vision in approximately 75%. VA ≥6/60 in 50–60% Complete retinal re-attachment, 80–85% (one operation).

■Risk : see Risks of vitrectomy (p. 532) and PRP (p.434). Retinal breaks during membrane dissection cause retinal detachment in 5–15%. Recurrent vitreous haemorrhage occurs in approximately 10%. Gas injection may be required at the time of surgery, to reduce the risk of retinal breaks causing retinal detachment.

RETINA SURGICAL 11 Chapter

Epiretinal membrane

Epiretinal Membrane

Background Thin preretinal membrane formed by fibroblastic cells. Most often idiopathic but may be secondary to retinal breaks, inflammation, diabetes, vitreous haemorrhage, retinal vascular occlusion, trauma, or any other disease that stimulates fibrosis. Sometimes called cellophane maculopathy, or preretinal gliosis. Macular pucker occurs when membrane contraction causes full-thickness retinal folds.

Symptoms Most patients are asymptomatic but the commonest symptom is distortion. VA reduction is usually mild (≥6/9 in two-thirds of cases) and nonprogressive.

Signs Typically cellophane-like, preretinal membrane causing fine wrinkles of the macula (Fig. 11.7). Thicker membranes are often associated with other disease. Bilateral in 25%. RPE changes and macular oedema may occur, and may indicate a worse surgical prognosis. Most have posterior vitreous detachment; if not, question the diagnosis.

History and examination Assess subjective severity and visual requirements. Record: near and distance VA, Amsler grid, lens status, vitreous attachment, retinal periphery and fellow eye disease.

Investigations Fluorescein angiography is not routinely required but may show vessel distortion and leakage. Optical

coherence tomography (OCT) can help exclude suspected vitreomacular traction syndrome.

Management

■Casualty : routine clinic referral.

■Clinic : discuss vitrectomy and membrane peel. The aim is to reduce distortion and improve VA.

Consent VA improves ≥2 lines in 74%, with 24% unchanged and 2% worse. Most patients report some improvement in metamorphopsia but few achieve entirely normal vision. Without surgery, VA is generally stable. Occasionally (<1%) the membrane separates spontaneously and VA improves. Explain the risks of vitrectomy (p. 532). Complications are reported to occur in 8% of cases.

Follow-up

■No surgery : discharge for annual optometrist review.

■Postoperative : G. chloramphenicol 0.5% q.d.s. 2 weeks, G. atropine 1% b.d. 2 weeks, G dexamethasone 0.1% q.d.s. 2 weeks then tail off over 3 weeks. Review subjective change in distortion, near and distance VA, lens opacity, residual membrane or wrinkling, and retinal periphery at day 1, 10, 30, 90, then discharge for annual dilated optometrist review. Membranes recur in 7%.

RETINA SURGICAL 11 Chapter

Vitreomacular traction syndrome

Vitreomacular Traction Syndrome

Background Partial vitreous detachment occurs but with points of residual attachment. These produce vitreomacular traction at one or more sites, and often also at the optic disc. This causes secondary macular oedema that may be aggravated by coexisting epiretinal membranes in 50% of cases.

Symptoms Blurred vision, metamorphopsia, photopsia, micropsia, and monocular diplopia.

History and examination Determine the duration and exact nature of symptoms and test with an Amsler grid. Use highpower macular lenses or a contact lens as vitreomacular traction can be hard to detect. Note any points of vitreous attachment. Exclude peripheral breaks that may be associated with epiretinal membranes.

Differential diagnosis Consider isolated epiretinal membrane, fullor partial-thickness macular hole, and other causes of macular oedema (p. 447).

Investigations Optical coherence tomography (OCT) is extremely helpful and shows vitreous attachment, foveal elevation, and macular oedema (Fig. 11.8). Fluorescein angiography is not routinely required but shows diffuse and extensive leakage and optic disc staining.

Treatment Spontaneous vitreous separation occurs in 11% but without treatment 64% lose 2 lines of VA over ≈6 years. Vitrectomy reduces retinal thickening in most cases and VA improves 2 lines or more in 44–75%, but falls by 2 lines in 0– 15%. Firm vitreoretinal adhesion coupled with macular oedema can result in macular hole formation during surgery.

Follow–up As for epiretinal membrane surgery (see previous page).

Macular hole

Macular Hole

Background A full-thickness retinal defect centred on the fovea. Commonest in late-middle-aged women. Usually idiopathic but may occur in high myopes, following trauma, or prolonged cystoid macular oedema.

Symptoms Reduced VA, distortion or incidental finding.

Signs

■Stage I : yellow spot with loss of normal foveolar depression.

■Stage II : round or curvilear full-thickness retinal defect (<350 μm).

■Stage III : full-thickness macular hole (FTMH). A pre-foveal operculum is common.

■Stage IV : FTMH with complete posterior vitreous detachment (Fig. 11.9). Associated findings include a grey cuff of subretinal fluid surrounding the hole, fine yellow-white deposits in the base of the hole, underlying RPE atrophy and occasionally retinal detachment in high myopes. VA is typically 6/24–6/60. Approximately 30% also have an epiretinal membranes (p. 536).

History and examination Record: duration and severity of symptoms, near and distance VA, lens and refractive status, vitreous attachment, stage of hole and check retinal periphery. Perform Watzke-Allen test using a macular lens: shine a narrow slit of light vertically across the hole; ask, ‘Is the line of light continuous, narrowed, or broken?’ If significantly narrowed

(> 50%) or broken, the test is positive, suggesting a FTMH rather than pseudoor lamellar hole. Repeat in the horizontal meridian.

Differential diagnosis Partial-thickness (lamellar) holes tend not to have cuff of fluid around the hole or RPE changes but they may progress to FTMH. Pseudohole an epiretinal membrane or macular cysts create the appearance of a FTMH.

Investigations Not routinely required.

■B-scan ultrasonography : may show posterior vitreous detachment if not visible clinically.

■Fluorescein angiography : RPE atrophy may give central hyperfluorescence with the cuff of subretinal fluid producing a hypofluorescent annulus.

■Ocular coherence tomography : if available, may confirm

Macular hole

Consent Stage III and IV: approximately 80% anatomic closure; 70% get 2 line VA improvement, 10% no change, 10% lose VA. Explain the risks of vitrectomy and gas injection (p. 532). Failed primary surgery may warrant re-operation.

Follow–up

■No surgery : discharge for annual optometrist review.

■Postoperative : G. Chloramphenicol 0.5% q.d.s. 2 weeks;

G. Atropine 1% b.d. 2 weeks; G. Dexamethasone 0.1% q.d.s. two weeks, then tail off over three weeks. Inspect for raised IOP, retinal breaks, visual and anatomic outcome, and cataract, at day 1, 7, 30, and 90, then discharge for annual optometrist review. The risk of contralateral FTMH is approximately 10–20%, but is unlikely if the vitreous is detached. Provide an Amsler grid.