Tractional Retinal Detachment 

Updated: Sep 20, 2018
Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD 

Overview

Background

Anytime subretinal fluid accumulates in the space between the neurosensory retina and the underlying retinal pigment epithelium (RPE), a retinal detachment occurs. Depending on the mechanism of subretinal fluid accumulation, retinal detachments traditionally have been classified into rhegmatogenous, tractional, and exudative.

A tractional retinal detachment (TRD) is the second most common type of retinal detachment after a rhegmatogenous retinal detachment (RRD).

Pathophysiology

In TRD secondary to proliferative vitreoretinopathy (PVR) and penetrating trauma, contractile vitreoretinal, epiretinal, intraretinal (very rarely), or subretinal membranes pull the neurosensory retina away from the RPE. PVR can be considered to represent an inappropriate or uncontrolled wound healing response. Microscopic examinations of these membranes have revealed their cellular composition. RPE cells, glial cells, fibrocytes, macrophages, and collagen fibrils are important components of these membranes. RPE cells are the major players in these membranes. They gain access to the vitreous cavity during retinal break formation. It has been shown that the amount of RPE cells in the vitreous cavity correlates with the size of the retinal breaks. The larger the break, the larger the amount of RPE cells intravitreally.

In addition, RPE cells also may be dispersed into the vitreous cavity by excessive cryotherapy, cryotherapy on bare RPE, and scleral indentation following cryotherapy. Once in the vitreous cavity, the RPE cells undergo morphological changes where they attain fibroblastlike activity, secreting growth factors that stimulate collagen and fibronectin production.

Cryotherapy also causes breakdown of the blood-ocular barrier, allowing serum to enter the eye. Serum components fibronectin and platelet-derived growth factor (PDGF) are strong chemoattractants for other RPE cells, astrocytes, and fibrocytes. Thus, one can understand the risk that vitreous hemorrhage poses in the chances of periretinal membrane formation. Once collagen sheets form, the individual cells pull on them, leading to TRD. Transforming growth factor beta (TGF-ß) is also a potent chemoattractant for monocytes and fibroblasts.[1] TGF-ß stimulates fibronectin synthesis and collagen contraction by RPE cells.[2, 3] Fibronectin may serve as a provisional matrix and scaffold for RPE cells in PVR membranes. It also induces conversion of RPE cells toward a fibroblastlike phenotype. In a rabbit model of PVR, decorin used as an adjuvant during vitrectomy reduced the amount of fibrosis and TRD.[4]

TRD may occur in a number of ocular pathologic conditions, such as proliferative diabetic retinopathy (PDR), sickling hemoglobinopathies, retinal venous obstructions, and retinopathy of prematurity (ROP), that are characterized by progressive retinal ischemia. Examples are shown in the images below.

Patient with a central retinal vein occlusion comp Patient with a central retinal vein occlusion complicated by neovascularization at the disc with subsequent tractional retinal detachment.
This patient underwent a scleral buckle for a rheg This patient underwent a scleral buckle for a rhegmatogenous retinal detachment. Now, the patient presents with proliferative vitreoretinopathy with a membrane tenting up and detaching the retina.
A patient with proliferative diabetic retinopathy A patient with proliferative diabetic retinopathy complicated by a tractional retinal detachment over the supertemporal arcade.

Progressive retinal ischemia leads to secretion of growth factors, especially vascular endothelial growth factor (VEGF). Neovascularization ensues, and the vitreous serves as a scaffold where strong vitreoretinal adhesions develop. With time, as the vitreous starts pulling away, a mechanical separation of the neurosensory retina from the underlying RPE occurs.

At the molecular level, VEGF is the main driver of angiogenesis and the resulting neovascularization. VEGF upregulates the profibrotic growth factor connective tissue growth factor (CTGF) in various cell types in the newly formed neovascular membranes. Increasing levels of CTGF inactivate VEGF, and when the equilibrium between these two factors shifts to a certain threshold ratio, the neovascular membranes become more fibrotic and less vascular. Fibrosis driven by excess CTGF leads to scarring and blindness.[5]

In the past few years, intravitreal anti-VEGF agents have gained popularity in the treatment of several diseases of the posterior segment of the eye characterized by macular edema and intraocular neovascularization such as proliferative diabetic retinopathy (PDR) and retinopathy of prematurity (ROP). In addition, they have been used as presurgical adjuvants in diabetic vitrectomies and ROP. Despite the advantages of such treatment, caution must be exercised in eyes with advanced PDR and ROP since a rapid involution of the fibrovascular proliferation may lead to the development or the progression of a tractional retinal detachment. In the largest study to date, the earliest development or progression of a TRD occurred 5 days after the injection. Timely surgery should be anticipated following intravitreal bevacizumab. Therefore, to be on the safe side, if bevacizumab is to be used as a vitrectomy adjunct, surgery should be performed no later than 4 days after injection.[6, 7]

Epidemiology

Frequency

United States

PVR is responsible for most failures of retinal reattachment surgery. It occurs in about 7% of eyes after retinal reattachment surgery. In 1 year, approximately 1600 new cases of PVR are seen.

Approximately 500 cases of blindness secondary to ROP are reported per year in the United States.

Mortality/Morbidity

Recent series have reported that the anatomical success rates of PVR are about 75-90%. However, the functional results are not that good since only about 40-50% of eyes attain 20/400 or better visual acuity.

ROP complicated by TRD is the leading cause of childhood blindness.

Diabetic retinopathy is the leading cause of blindness in the working age group. In the 1960s, prior to the advent of laser photocoagulation, up to 50% of patients with PDR were legally blind. With new techniques, currently only 5% of patients with PDR progress to legal blindness.

Race

TRD related to sickle cell disease occurs mainly in blacks.

Sex

No studies exist that specifically refer to the incidence of TRD according to gender. However, it is well known that men are more susceptible to penetrating trauma than women.

Age

The incidence of TRD according to age depends on the cause.

Prognosis

Visual prognosis depends on the underlying cause of TRD.

Anatomical success rates for retinal reattachment surgery for PVR are anywhere from 75-90% of eyes. However, visual results are poor, since only about 40-50% obtain a visual acuity of 20/400 or better.

The results after ROP surgery are very poor but better than the natural history (no light perception).

For PDR, series by Rice et al, Thompson et al, and Williams et al report 70-80% of eyes attain 5/200 or better visual acuity with 40% achieving 20/100 or better.[8, 9, 10]

Patient Education

Patients with diabetes must be aware that a fully dilated eye examination by a competent ophthalmologist should be performed at least once a year. Depending on the presence and degree of retinopathy, the patient may need to be seen on a more frequent basis.

Patients should be educated about the importance of good glycemic, hypertensive, and lipemic control.

 

Presentation

History

Vitreoretinal traction develops insidiously in most cases.

The visual field defect progresses slowly and may become stationary for months or years.

If the macula becomes involved, the patient will experience a drop in vision.

Physical

The detachment has a concave configuration.

The subretinal fluid is shallower than in RRD and often does not extend to the ora serrata.

The highest elevation of the retina occurs in sites of vitreoretinal traction.

Retinal mobility is severely reduced, and shifting fluid is absent.

Causes

See the list below:

  • PDR

  • ROP

  • Penetrating trauma

  • Proliferative sickle retinopathy

  • PVR

  • Retinal venous occlusions

Complications

See the list below:

  • Retinal redetachment

  • Vitreous hemorrhage

  • Phthisis bulbi

 

DDx

 

Workup

Laboratory Studies

The diagnosis of a TRD is made clinically. Further laboratory workup is unnecessary.

Imaging Studies

In eyes with vitreous hemorrhage, a B-scan ultrasound is a useful adjunct to evaluate the presence or absence of retinal detachment.

Histologic Findings

The same findings as those found in RRD (see Retinal Detachment, Rhegmatogenous), that is, photoreceptor outer segment loss in the acute cases. Following successful retinal reattachment, regeneration of the outer segments may occur. In chronic detachments, atrophy of the entire photoreceptor layer, cystic degeneration, macrocyst formation, demarcation lines, and even rubeosis iridis may be seen.

In addition, TRDs have periretinal proliferation. Light and electron microscopy have revealed the composition of the periretinal membranes. These are composed of RPE cells, astrocytes, fibrocytes, monocytes, and collagen fibrils.

 

Treatment

Medical Care

Currently, no role exists for medical care in the treatment of TRD.

Surgical Care

Depending on the underlying cause and extent of the TRD, surgical intervention is offered to patients. For instance, a patient with TRD secondary to PDR that does not threaten the macula probably can be monitored closely. The main surgical goal in all these cases is to relieve vitreoretinal traction. Traction may be relieved with scleral buckling techniques and/or with vitrectomy.

In certain cases, combined RRD and TRD may be present. Usually, the retina becomes detached from the vitreoretinal traction. With further traction, small breaks may occur causing a combined TRD-RRD. In these cases, the surgical goal is to identify all the breaks and to close them in addition to the relief of vitreoretinal traction.

Tractional Retinal Detachment Due to Proliferative Vitreoretinopathy

In TRD secondary to PVR, usually a broad circumferential element, such as a 287 buckle, is placed. A decision is made whether the crystalline lens needs to be sacrificed. A complete vitrectomy follows. Inside-out (posterior to anterior) forceps (not pick) membrane peeling is the preferred dissection method with or without perfluorocarbon liquid injection. Perfluorocarbon liquid may be injected at the surgeon's discretion to stabilize the posterior retina. If residual traction remains, subretinal membranes may need to be excised if causing traction. If necessary, a relaxing retinectomy is created. A fluid-air exchange is performed. Endophotocoagulation is followed by either air-silicone oil exchange or air-gas exchange. If perfluorocarbon liquids are not used, the dissection starts anteriorly and proceeds posteriorly.

A randomized controlled clinical trial of a perioperative infusion of 5-fluorouracil and low molecular weight heparin was not able to demonstrate a better surgical outcome in eyes with established PVR. There has been a recent interest in using methotrexate as an antiproliferative agent.[11, 12]

Tractional Retinal Detachment Due to Proliferative Diabetic Retinopathy

In TRD secondary to PDR, several surgical techniques have been developed. A scleral buckle usually is not used unless anterior breaks are present.

A central vitrectomy is performed with the vitrector clearing the axial opacities and the cortical vitreous gel. A large opening is created in the posterior hyaloid until vitreoretinal adhesions are encountered. Segmentation and/or delamination of these adhesions (as described by Charles) are used for virtually all diabetic TRD.

Delamination refers to the separation of the retina from the extraretinal proliferation. This dissection proceeds from posterior to anterior. Fibrovascular tissue often bridge separate retinal zones. Segmentation refers to cutting of the fibrovascular tissue bridge into small separate islands of tissue.

Care must be given to create as few iatrogenic breaks as possible. If breaks are identified, usually fluid-air exchange with photocoagulation reattaches the retina. Breaks should be marked with diathermy, so they are identified easily in the air-filled eye. The incidence of RRD in patients who underwent vitrectomy for PDR has been reported to be 4.3%. Intraocular bleeding also must be monitored closely. Diathermy to active neovascular fronds may be necessary.

Other techniques include the en bloc dissection. En bloc is a name applied to outside-in delamination where the vitreous is used to pull on the epiretinal membrane. Outside-in causes more retinal breaks than inside-out, making it a dangerous maneuver.

Recent advances in small-gauge instrumentation have facilitated the peeling of membranes in these cases, in many cases obviating the need for intraocular picks and scissors.[13, 14, 15, 16, 17, 18]

Intravitreal bevacizumab has been reported as a preoperative adjunct in vitrectomy for PDR. Bevacizumab seems to reduce the bleeding associated with the segmentation and delamination of fibrovascular membranes. However, in eyes with severe ischemia, the neovascularization regresses rapidly, but the resulting fibrous scar tissue may lead to the development or progression of TRD. Therefore, caution should be exercised when injecting these eyes, and patients should be scheduled for surgery days, and not weeks, after the injection.

Anti-VEGF agents such as bevacizumab have been used as adjuncts to vitrectomy. The advantages of using preoperative bevacizumab includes faster surgery and reduced risk of intraoperative bleeding, which facilitates membrane dissection.[19, 20, 21, 22] Care must be taken because it has been reported that, in very ischemic eyes, TRD may occur or progress shortly following intravitreal bevacizumab.[20, 21] It is speculated that rapid neovascular involution with accelerated fibrosis and posterior hyaloidal contraction as a response to decreased levels of VEGF is responsible for this phenomenon. In this retrospective series, the time from injection to TRD was a mean of 13 days, with a range of 3-31 days.[20] Therefore, the time between bevacizumab injection and vitrectomy should not exceed 3 days.

Tractional Retinal Detachment Due to Retinopathy of Prematurity

The treatment of TRD secondary to ROP depends on the stage of the disease.

Although many vitreoretinal surgeons advocate an encircling band for stage 4A ROP, no scientific evidence is available that supports its efficacy. In stage 4B, vitrectomy is recommended. It is currently unclear if lens-sparing vitrectomy has any advantages over lensectomy.

For stage 5 ROP, visual and anatomical results have been disappointing, making some surgeons abandon surgery for these cases. Others have tried vitrectomy and lensectomy with or without scleral buckling. In these cases, a 2-port vitrectomy technique is recommended since the small size of the eye and orbit limits ocular manipulation if a 3-port technique is used. The use of intravitreal triamcinolone as a postoperative adjuvant might improve the rate of retinal reattachment after vitrectomy.

A recent case series of aggressive posterior ROP suggested that early vitrectomy with lensectomy in these cases is effective in preventing TRD.

Special attention must be given to avoid iatrogenic retinal breaks because of the poor prognosis associated with this complication. The goal of surgery is to obtain macular reattachment.

Consultations

Patients with TRD should be referred to an experienced vitreoretinal surgeon for further management.

Prevention

Proliferative vitreoretinopathy

Extensive cryotherapy, cryotherapy over bare RPE, and scleral depression after cryotherapy should be avoided because this will disperse RPE cells into the vitreous cavity. Cryotherapy also causes breakdown of the blood-ocular barrier, allowing serum (containing various growth factors believed to be stimulatory to the formation of PVR) to enter the eye.

A double-masked, prospective, randomized, placebo-controlled clinical trial reported that adjuvant therapy with 5-fluorouracil and low molecular weight heparin does not improve anatomical and visual success rates in retinal detachments with preexisting PVR. Furthermore, it is associated with worse visual outcomes in cases with macula-sparing retinal detachment.

Proliferative diabetic retinopathy

Patients with diabetes should be monitored closely and treated with aggressive panretinal photocoagulation when indicated.

Retinopathy of prematurity

Screening protocols should be monitored, and patients should be treated with laser or cryotherapy as indicated.

Further Outpatient Care

Certain eyes that undergo vitreoretinal surgery have an intraocular gas bubble to serve as internal tamponade. Depending on the gas used and the location of the breaks, the surgeon instructs the patient to maintain a certain head position for a limited time.

Further Inpatient Care

Most vitreoretinal procedures currently are performed in an ambulatory setting.

Inpatient & Outpatient Medications

Postoperative medications usually include a topical corticosteroid, a topical cycloplegic, and a topical antibiotic. The intraocular pressure is monitored and controlled accordingly.

 

Medication

Medication Summary

TRDs are considered to be surgical diseases. However, experimental drugs have been used in numerous protocols to try to prevent PVR at different stages of the disease process. Among the drugs studied are heparin and its low molecular weight derivatives, corticosteroids and nonsteroidal anti-inflammatory agents, antimetabolites, and retinoic acid. Most of these agents have been shown to reduce retinal proliferation. However, such issues as drug toxicity, drug delivery, and drug duration of action remain without an ideal solution.