Tractional retinal detachment (TRD) is a retinal detachment that occurs when strong vitreous traction is exerted on the retina in the absence of complete posterior vitreous detachment. It is a non-rhegmatogenous retinal detachment caused by proliferative tissue on the retina or vitreous traction. The detachment is often localized, flat or tent-shaped, and characteristically has little mobility.
TRD is broadly classified into the following two types based on the cause.
Traction by fibrovascular membranes (including neovascularization): Representative diseases are proliferative diabetic retinopathy (PDR), retinal vein occlusion (RVO), and retinopathy of prematurity (ROP). It is based on neovascularization in response to intraocular ischemia, and contraction of the fibrovascular membrane generates traction.
Vitreoretinal traction without neovascularization: Representative diseases are vitreomacular traction syndrome and perforating ocular trauma. It is based on proliferation after inflammation or trauma.
Retinal detachment is generally classified into three types: rhegmatogenous, tractional, and exudative. Tractional detachment is clinically distinguished from rhegmatogenous (which is bullous and mobile) and exudative detachment as a localized, immobile detachment. Some cases may have a concurrent retinal break, which is called combined tractional-rhegmatogenous RD. Combined RD is a more urgent condition and its management differs from that of pure tractional RD.
Proliferative vitreoretinopathy (PVR) is a proliferative process that occurs secondarily after rhegmatogenous retinal detachment surgery and can also be a cause of TRD.
Rhegmatogenous RD occurs when liquefied vitreous flows into the subretinal space through a retinal break, presenting as a bullous, mobile detachment. Tractional RD occurs when the retina is pulled by proliferative membranes or vitreous contraction, presenting as a tent-shaped, immobile detachment. Combined tractional-rhegmatogenous RD also exists. Differentiation is made by fundus examination, OCT, and B-scan ultrasonography.
Subjective symptoms of TRD vary greatly depending on the location and extent of the detachment.
In tractional retinal detachment (TRD) associated with diabetic retinopathy (DR), vitreous hemorrhage often occurs, which can cause sudden vision loss1).
The characteristic morphological findings of TRD are shown below.
Tent-shaped Detachment
Mechanism: Formed when traction occurs at the base of new vessels (epicenter) or along retinal vessels.
Features: The detached area has a reverse-arch (tent-like) shape. It is immobile and often limited in height. Typical in early to mid-stage PDR.
Tabletop Detachment
Mechanism: Formed when adhesion between the fibrovascular membrane and retina is extensive. Also called Mount Fuji type.
Features: Forms a broad, flat detachment surface. It is immobile, and if it covers the entire macula, the visual prognosis is poor.
Assessment of mobility: The lack of mobility in tractional RD is an important finding. If the detachment has a dome shape or mobility, concurrent rhegmatogenous RD (combined RD) should be considered.
Presence of fibrovascular membrane: In PDR-derived TRD, a membrane structure formed by fusion of retinal new vessels and fibrous tissue is observed. The activity of the membrane (richness of vascular components, bleeding tendency) affects surgical difficulty.
Complicated vitreous hemorrhage: In proliferative diabetic retinopathy, bleeding from fibrovascular membranes may obscure the view. In such cases, B-mode ultrasound is necessary because fundus examination is difficult.
Tractional retinoschisis: When strong traction occurs on the retinal surface in proliferative diabetic retinopathy, the inner and outer layers of the retina may separate, resulting in retinoschisis. The surface shape is tent-like, and OCT is useful for diagnosis.
TRD is caused by the following underlying diseases.
1. Proliferative Diabetic Retinopathy (PDR): The most common cause of TRD. Neovascularization forms as compensation for retinal ischemia, and fibrovascular membranes proliferate and contract on the retina, leading to TRD. The Diabetic Retinopathy Clinical Practice Guidelines (1st edition) clearly state that tractional retinal detachment is one of the serious complications of PDR 1).
2. Retinopathy of Prematurity (ROP): TRD occurs in Stage 4 (partial TRD) and Stage 5 (total TRD) 4). In the immature retina with avascular zones where retinal vessels have not developed, the postnatal hyperoxic environment causes relative ischemia, leading to neovascularization.
3. Penetrating Ocular Trauma: Inflammatory cell infiltration from the perforation site and breakdown of the blood-retinal barrier (BRB) lead to intraocular proliferation, resulting in membrane formation and traction.
4. Proliferative Vitreoretinopathy (PVR): Proliferation that occurs secondarily after rhegmatogenous retinal detachment surgery may add a tractional component, leading to a TRD-like condition.
5. Retinal Vein Occlusion (RVO): In severe cases with neovascularization, TRD can occur through a mechanism similar to PDR.
6. Others: TRD may also occur in Eales disease (idiopathic peripheral periphlebitis), sickle cell disease, and some cases of Coats disease.
The following table summarizes each causative disease and risk factors.
| Risk Factors | Associated Disease |
|---|---|
| Duration of diabetes, poor glycemic control | PDR |
| Low birth weight, preterm birth (gestational age <32 weeks) | ROP |
| Perforating ocular trauma | Post-traumatic TRD |
| History of rhegmatogenous retinal detachment surgery | PVR |
| Panretinal photocoagulation not performed or incomplete | PDR |
| Retinal vein occlusion | TRD due to ischemic RVO |
For anti-VEGF therapy for retinopathy of prematurity, refer to the guidelines of the Japan Retinopathy of Prematurity Study Group 7).
Fundus observation using an indirect ophthalmoscope or slit-lamp biomicroscope (with a pre-corneal lens) is the basis for diagnosing TRD.
OCT is particularly effective for diagnosing tractional retinoschisis. It can visualize the tent-shaped surface contour caused by traction on tomographic images. It allows quantitative assessment of the degree of macular traction, separation of inner and outer retinal layers, and the extent of detachment progression toward the macula.
This is an essential examination when fundus observation is not possible due to vitreous hemorrhage or severe cataract. It can assess the presence, extent, morphology, and degree of traction of retinal detachment. Proliferative membranes may appear as high-intensity echoes.
FA is useful for assessing neovascular activity and detecting non-perfusion areas (NPAs) 1). In PDR-related TRD, understanding the extent of non-perfusion areas preoperatively helps in planning intraoperative photocoagulation.
The differential diagnosis of conditions similar to TRD is summarized below.
| Differential Diagnosis | Features | Mobility | Morphology |
|---|---|---|---|
| Rhegmatogenous RD | Retinal break present | Present | Bullous |
| Tractional RD | Proliferative membrane present | None | Tent-shaped or tabletop |
| Exudative RD | No tear or proliferative membrane | None to mild | Smooth dome-shaped |
| Combined TRD-RRD | Tear + proliferative membrane | Present | Mixed tent-shaped and bullous |
B-mode ultrasound is essential. It can assess the presence, extent, and degree of traction of retinal detachment. If PDR is suspected as the cause of vitreous hemorrhage, fundus findings of the fellow eye are also used as a reference for diagnosis. OCT is used adjunctively when observation near the retinal surface is possible.
The surgical indications for TRD are as follows.
| Condition | Management |
|---|---|
| Tractional retinal detachment threatening the macula | Surgical indication1, 2) |
| Combined tractional and rhegmatogenous retinal detachment (combined RD) | Surgical indication (more urgent)1, 2) |
| Proliferative membrane that may cause macular displacement | Consider surgery1) |
| Localized TRD outside the macula (no progression) | Observation possible |
For localized TRD outside the macula, if there is no enlargement of the detachment or macular displacement, observation is possible with regular fundus examination and OCT monitoring. However, if signs of progression are observed, early surgery should be considered1).
The definitive treatment for TRD is traction removal via vitrectomy. In recent years, 25G and 27G microincision vitrectomy surgery (MIVS) has become mainstream, and surgery under a wide-angle viewing system is standard1).
The basic surgical procedure is as follows.
Preoperative intravitreal anti-VEGF injection may help reduce intraoperative bleeding, iatrogenic breaks, and surgical time 3). It is considered in PDR-associated TRD with high fibrovascular membrane activity.
The surgical approach for TRD associated with retinopathy of prematurity varies depending on the stage4).
Anti-VEGF therapy may be used as first-line treatment for severe ROP7), but vitrectomy is the principle for Stage 4-5 TRD.
If there is no risk of progression to the macula, observation is possible. However, if there is an enlarging detachment or proliferative membranes that may cause macular ectopia, earlier surgery should be considered. Regular fundus examination and OCT monitoring for progression are important.
TRD derived from proliferative diabetic retinopathy develops through the following stages.
Pathology of TRD from PDR
The chain of ischemia → VEGF → new blood vessels forms the basis.
Contraction of the fibrovascular membrane generates traction on the retina, leading to TRD. Cytokine leakage due to breakdown of the blood-retinal barrier (BRB) promotes proliferation.
Pathology of TRD from ROP
Immaturity of retinal vessels → avascular zone → ischemia → new blood vessels form the basis.
The relative ischemia caused by the high-oxygen environment after birth leads to fibrovascular proliferation on the ridge, which extends into the vitreous, resulting in Stage 4-5 TRD.
The basis of TRD is disruption of the blood-retinal barrier (BRB). When the BRB is disrupted, the intraocular inflammatory and angiogenic environment intensifies, and fibrovascular proliferation progresses. RPE, glial cells, macrophages, fibroblasts, and others are involved in the formation of proliferative membranes 9).
Not only RPE but also glial cells, macrophages, fibroblasts, and others are complexly involved in the proliferative membrane. Contraction of collagen causes traction on the retina, leading to the development of TRD.
In TRD after penetrating ocular trauma, intraocular proliferation progresses due to inflammatory cell infiltration from the perforation wound and BRB disruption. Proliferation of fibroblasts and RPE forms a proliferative membrane, which contracts and causes traction, leading to TRD.
The Diabetic Retinopathy Vitrectomy Study (DRVS), which examined the efficacy of early vitrectomy for severe diabetic vitreous hemorrhage, provides evidence that forms the basis of TRD management. In type 1 diabetes with severe vitreous hemorrhage, the proportion achieving corrected visual acuity of 20/40 or better at 2 years was 25% in the early vitrectomy group (vs. 15% in the observation group), and in type 1 diabetes, 36% vs. 12%, showing a significant difference 5). No significant difference was observed in type 2 diabetes 5).
In a trial comparing intravitreal aflibercept injection and vitrectomy plus panretinal photocoagulation (PRP) for diabetic vitreous hemorrhage, no significant difference in visual improvement was observed at 24 weeks. However, resolution of vitreous hemorrhage was faster in the surgery group (4 weeks vs. 36 weeks) 2).
A meta-analysis examining the usefulness of preoperative anti-VEGF administration reported a reduction in intraoperative bleeding and iatrogenic tears 3). However, it has been pointed out that traction may temporarily worsen after anti-VEGF injection, and early surgery within 1–2 weeks after injection is recommended 2).
With the widespread use of 25G and 27G systems and wide-angle viewing systems, the indications for minimally invasive vitrectomy for PDR-derived TRD have expanded 1). Small-incision techniques contribute to reduced postoperative inflammation and faster recovery, and their application in outpatient surgery is increasing 8, 9).
In DRCR Protocol S, anti-VEGF (ranibizumab) showed non-inferiority to PRP at 2 years 2). However, there was no significant difference in the rate of progression to TRD, and anti-VEGF alone cannot manage existing TRD. Anti-VEGF may be considered for TRD prevention, but once TRD develops, vitrectomy is the definitive treatment.
Improvement of TRD with anti-VEGF injections alone is generally not expected. Anti-VEGF is effective for regression of neovascularization but cannot control contraction of existing fibrous proliferative membranes; some reports even indicate worsening of traction after injection 2). The principle treatment for TRD is vitrectomy. Preoperative anti-VEGF administration may be useful in some cases, potentially reducing intraoperative bleeding and iatrogenic breaks 3).
