Tractional Retinal Detachment

Detachment of the retina caused by contraction of fibrovascular or fibrocellular membranes on the retinal surface or in the vitreous that pull the neurosensory retina away from the retinal pigment epithelium, without a primary retinal break.

• Causes:
  • Proliferative diabetic retinopathy (the most common cause): neovascular fronds grow along the posterior hyaloid and contract after vitreous separation.
  • Retinopathy of prematurity (stage 4 and 5).
  • Sickle cell retinopathy (proliferative stage), Eales disease, retinal vein occlusion with neovascularisation, and radiation retinopathy.
  • Penetrating ocular trauma with vitreous incarceration, and previous retinal surgery with proliferative vitreoretinopathy.
  • Familial exudative vitreoretinopathy, ocular toxocariasis, persistent fetal vasculature, and incontinentia pigmenti.
• Traction produces a concave, taut retinal surface with immobile folds; secondary retinal breaks (combined tractional-rhegmatogenous detachment) convert the picture to a convex mobile detachment that progresses rapidly.

• Painless progressive loss of vision or field, floaters from vitreous haemorrhage, or distortion; some are discovered incidentally. Slow progression over weeks to months is typical.
• Fundus: fibrovascular membranes (white-grey avascular tissue or "tent"-shaped traction along arcades), retinal folds and distortion of vessels, taut retinal surface elevated in a concave contour, with little shifting subretinal fluid, and a smooth immobile retina; the detachment seldom extends to the ora serrata.
• Macula involvement causes central vision loss; vitreous haemorrhage often accompanies (the fundus view is poor).
• Combined tractional-rhegmatogenous: convex retina, moving fluid, tobacco dust, and rapid progression with the break at the edge of traction.
• Associated active neovascularisation, rubeosis iridis, and neovascular glaucoma in advanced disease.

• Dilated fundus examination with indirect ophthalmoscopy and slit lamp biomicroscopy using contact or non-contact lenses.
• Optical coherence tomography to define macular traction, vitreomacular interface, and macular involvement.
• B-scan ultrasound for dense vitreous haemorrhage: shows membranes, retinal elevation, and whether the posterior hyaloid is attached.
• Fluorescein angiography for ischaemia, active neovascularisation, and fibrovascular activity.
• Systemic control: glycated haemoglobin, blood pressure, lipids, renal function, and pregnancy status in diabetic patients.

• Observation with regular imaging is acceptable for tractional detachments confined to the periphery or not threatening the fovea, along with optimal systemic control and panretinal photocoagulation (1200 to 2000 burns, 500 micrometre spots, 0.1 seconds, 200 to 400 mW) to induce regression of neovascularisation.
• Intravitreal anti-vascular endothelial growth factor (bevacizumab 1.25 mg in 0.05 mL or aflibercept 2 mg in 0.05 mL) 3 to 7 days before surgery reduces intraoperative bleeding; avoid delay beyond 7 to 10 days because contraction of fibrovascular tissue can cause progression of traction ("crunch").
• Pars plana vitrectomy (23, 25 or 27 gauge): indicated for macula-threatening or macula-involving tractional detachment, combined tractional-rhegmatogenous detachment, non-clearing vitreous haemorrhage with traction, and fibrovascular proliferation with progressive worsening.
  • Steps: core vitrectomy, relief of anteroposterior and tangential traction by segmentation and delamination of membranes (scissors, forceps, bimanual technique), removal of the posterior hyaloid, endolaser panretinal photocoagulation, treatment of iatrogenic breaks, and tamponade with gas (20 percent sulphur hexafluoride or 14 percent perfluoropropane) or silicone oil (1000 or 5000 centistokes) in complex cases.
• Cataract surgery as needed, treatment of neovascular glaucoma, and control of diabetes.
• Postoperative care: topical antibiotic and steroid, intraocular pressure monitoring, positioning as directed, repeat laser as needed.
• Outcomes: anatomical success 80 to 90 percent; visual recovery is limited by macular ischaemia, prolonged detachment, and recurrent bleeding. Risks include recurrent vitreous haemorrhage, redetachment, proliferative vitreoretinopathy, neovascular glaucoma and phthisis.