Traction Retinal Detachment (TRD)

Definition & Pathophysiology

Etiology

Clinical Features

Symptoms

• Visual loss or visual field defect
• May be asymptomatic, especially when extramacular

Signs (Key Features)

Fundus photograph: Tractional retinal detachment — note the fibrovascular membranes (yellow-green) pulling the retina, with the optic disc displaced

• The detached retina has a concave, tent-like configuration with a smooth surface (cf. rhegmatogenous RD which is convex/bullous)
• Cellular and vitreous fibrovascular membranes are visible exerting traction on the retina
• Retinal striae (folds) radiate from areas of traction
• The retina is immobile (does not shift with eye movement)
• Detachment rarely extends to the ora serrata
• A mild relative afferent pupillary defect (RAPD) may be present in large detachments
• If a retinal tear develops within the TRD, it converts to a combined TRD/rhegmatogenous RD — now convex and more bullous (urgent)

Comparison with Other Types of Retinal Detachment

Workup

1. Slit lamp examination — assess lens status, neovascularization of the iris (rubeosis), and posterior vitreous detachment (PVD)
2. Indirect ophthalmoscopy with scleral depression of both eyes; slit lamp + 90D or widefield lens for peripheral breaks
3. B-scan ultrasound — essential when media opacities (vitreous hemorrhage, cataract) are present
4. OCT — identifies tractional membranes, differentiates membranes from detached retina, essential for evaluating macular involvement

Management

Observation

• Extramacular TRDs (not involving the fovea) can often be observed — they tend to remain stationary for prolonged periods
• Decision depends on: etiology, fellow eye status, extent/location of traction

Surgical Indications

1. TRD threatening or involving the macula — treat without delay
2. Combined TRD + rhegmatogenous RD — treat urgently
3. Dense, non-clearing vitreous hemorrhage preventing adequate visualization or laser
4. Macular epiretinal membranes or vitreomacular traction causing significant symptoms
5. Severe fibrovascular proliferation unresponsive to laser/anti-VEGF

Surgical Approach: Pars Plana Vitrectomy (PPV)

• The mainstay of treatment for TRD
• Goals: remove vitreous, segment and delaminate fibrovascular membranes, relieve traction
• Combined with endolaser photocoagulation (PRP) in diabetic cases
• Intravitreal anti-VEGF agents (e.g., aflibercept, bevacizumab) may be given preoperatively (1–7 days before surgery) to reduce intraoperative bleeding from fibrovascular membranes
• DRCR.net Protocol AB: initial vitrectomy + PRP leads to faster visual recovery vs. aflibercept, with similar 2-year outcomes

TRD secondary to branch retinal vein occlusion: preoperative fibrovascular band with foveal-involving detachment confirmed on OCT (a,c); post-vitrectomy with traction released (b,d); 5-year stable OCT follow-up (e,f)

Follow-Up

• After surgery, patients are typically seen at 1 day → 1 week → 1 month → 2–3 months → every 6–12 months
• TRD follow-up schedule depends on underlying etiology and patient factors
• Retinal specialist referral is required for all cases

Key Points to Remember

• TRD is always secondary to another process — treat the underlying cause (e.g., control DM, treat PDR with PRP)
• The characteristic concave, immobile, smooth surface distinguishes TRD from RRD
• A TRD that develops a retinal break becomes a combined TRD/RRD, which behaves differently (more bullous, requires urgent repair)
• Macular involvement is the surgical tipping point — extramacular TRDs are often observed; macular TRDs require prompt vitrectomy
• Young type 1 diabetics have more aggressive PDR and benefit from earlier intervention

ETDRS — Early Treatment Diabetic Retinopathy Study

Overview

1. When should photocoagulation be initiated in diabetic retinopathy — early (before high-risk PDR develops) or deferred?
2. Is aspirin effective in altering the course of diabetic retinopathy?

Study Design

Key Findings

1. Photocoagulation Timing

Key conclusion: "In eyes with CSMO, initiate focal photocoagulation. In eyes with high-risk PDR, initiate PRP promptly. In eyes with less severe retinopathy, careful observation is acceptable if follow-up is reliable."

2. Aspirin

• Aspirin 650 mg/day did NOT affect the progression of diabetic retinopathy — neither beneficial nor harmful on retinopathy outcomes
• Aspirin did not increase risk of vitreous hemorrhage
• Therefore: aspirin is NOT contraindicated in diabetic patients who require it for cardiovascular indications — do not withhold it to protect the eyes

3. ETDRS Classification of Diabetic Retinopathy

4. Clinically Significant Macular Oedema (CSMO)

1. Retinal thickening within 500 μm (≈ ⅓ disc diameter) of the centre of the macula
2. Hard exudates within 500 μm of the centre with adjacent retinal thickening (the thickening itself may extend beyond 500 μm)
3. Retinal thickening ≥1 disc area, any part of which is within 1 disc diameter of the centre of the macula

CSMO is an indication for focal/grid laser photocoagulation, regardless of the level of visual acuity. (In contemporary practice, centre-involving CSMO is preferentially treated with anti-VEGF agents — DRCR.net Protocol I and T.)

The 4-2-1 Rule (Severe NPDR) — ETDRS Derived

• 4 quadrants with severe intraretinal haemorrhages
• 2 quadrants with venous beading
• 1 quadrant with IRMA

ETDRS Visual Acuity Chart

• Uses Sloan optotypes on a 5×5 grid
• Balanced rows: each row has equivalent legibility across letters
• Calibrated for 4 metres
• 5 letters per row; each letter = 1 logMAR unit ÷ 5 = 0.02 logMAR per letter
• Allows more precise measurement than Snellen charts — preferred for clinical trials

Clinical Impact & Legacy

Exudative (Serous) Retinal Detachment — 10 Marks

Definition

Pathogenesis

• Breakdown of the outer blood-retinal barrier (RPE or choriocapillaris) → excessive fluid leakage into the subretinal space
• RPE pumping overwhelmed by inflammatory, neoplastic, or vascular processes
• Choroidal venous outflow obstruction (e.g., nanophthalmos, uveal effusion syndrome)

Aetiology / Causes

Neoplastic

• Choroidal malignant melanoma (most important — must be excluded first)
• Choroidal metastases (breast, lung most common)
• Choroidal haemangioma (circumscribed or diffuse)
• Retinal capillary haemangioblastoma
• Multiple myeloma

Key rule: An intraocular tumour should be considered the cause of an exudative RD until proved otherwise. — Kanski's

Inflammatory

• Vogt-Koyanagi-Harada (VKH) syndrome — multifocal bilateral exudative RD
• Posterior scleritis — serous macular detachment
• Sympathetic ophthalmia
• Other posterior uveitis

Vascular

• Choroidal neovascularization (CNV / wet AMD)
• Coats disease — massive lipid exudation
• Malignant hypertension / hypertensive choroidopathy
• Pre-eclampsia / toxaemia of pregnancy
• Familial exudative vitreoretinopathy (FEVR)

Idiopathic / Structural

• Bullous central serous chorioretinopathy (CSCR) — rare, more often pigment epithelial detachment
• Uveal effusion syndrome — bilateral, associated with nanophthalmos/high hyperopia; dilated episcleral vessels; leopard-spot RPE changes
• Congenital: optic pit, morning glory syndrome, choroidal coloboma

Iatrogenic

• Post-retinal detachment surgery
• Post-panretinal photocoagulation

Clinical Features

Symptoms

• Visual field defect — varies with head position (pathognomonic feature)
• Visual loss — variable severity
• Visual changes shift with posture (inferior field loss when upright → posterior field/macular when supine)
• No photopsia — because there is no vitreoretinal traction
• Floaters if there is associated vitritis
• May be bilateral depending on cause (e.g., VKH, malignant HTN)

Signs

Exudative RD — smooth, dome-shaped elevation of the retina without corrugation. Note absence of demarcation lines.

Exudative RD in VKH: multifocal pale elevated areas representing serous detachments peripapillary and parafoveal, with hyperaemic optic disc (papillitis)

Serous macular detachment in posterior scleritis (A) resolving completely after systemic prednisolone (B) — confirmed on OCT

Differential Diagnosis

Investigations / Workup

1. Fundus examination — indirect ophthalmoscopy; scleral depression to rule out hidden break
2. B-scan ultrasonography — identify underlying choroidal tumour, posterior scleritis ("T-sign" of fluid in Tenon's capsule), choroidal thickness; assess shifting fluid
3. Intravenous fluorescein angiography (IVFA) — demonstrates pooling of dye in subretinal space (smokestack/inkblot pattern in CSCR); identifies leakage source; highlights CNV
4. OCT — confirms subretinal fluid; identifies CNV, pigment epithelial detachments; quantifies extent
5. Indocyanine green angiography (ICGA) — hypofluorescent spots in VKH; choroidal polyps in PCV; choroidal tumour vasculature
6. Systemic workup — blood pressure, renal function, FBC; imaging for primary malignancy (chest X-ray/CT); inflammatory markers (ESR, CRP); skin/hair/neurological exam (VKH)

Treatment

Some cases (e.g., VKH, posterior scleritis) resolve completely with systemic steroids. Others (neoplastic) require specific oncological treatment. The prognosis depends entirely on the underlying aetiology and promptness of treatment.

Key Points for Exam

1. No break, no traction — defines exudative RD
2. Shifting fluid is pathognomonic
3. Smooth, convex, very mobile retina
4. Tumour must be excluded first — especially choroidal melanoma
5. No photopsia — distinguishes from RRD
6. Treatment = treat the cause; surgery has no primary role
7. Leopard spots after resolution indicate prior exudative RD (e.g., VKH, uveal effusion)