Tractional retinal detachment

Tractional retinal detachment

Description, Causes and Risk Factors:

Abbreviation: TRD.

The retina is responsible for creating the images that we see. Its neurosensory tissue lines the back of the eye and functions very similar to film in a camera. Ninety-five percent of the retina, called the peripheral retina, is responsible for side vision. The other five percent is the very center of the retina, called the macula. It is responsible for detailed vision for daily functions like reading and recognizing faces.

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 retinal detachment (RRD), tractional retinal detachment (TRD), and exudative retinal detachment (ERD).

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

There are three types of TRD: the flap tear, the tear along lattice lesions, and an operculated tear. In the classic flap (or horseshoe) tear, the retina is pulled incompletely free and forms a triangular appearance. The apex of the tear is still attached to the mobile vitreous and points towards the posterior pole. The base of the triangle parallels the vitreous base. The mobile vitreous acts to further tear the retina and separate it from the RPE. If the tear bridges a blood vessel, there can be a subsequent vitreous hemorrhage. A similar retinal tear occurs at the posterior border of lattice lesions due to the same forces, but does not have the triangular appearance of the flap tear. If an area of retinal tissue is pulled completely free by the vitreous, it is considered an operculated tear. The retinal tissue, now termed an operculum, is seen to float in the vitreous above the retinal tear.

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. 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 (retinal pigment epithelium) 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.

Common Risk Factors:

    Proliferative diabetic retinopathy (PDR).

  • Retinopathy of prematurity (ROP).

  • Proliferative sickle retinopathy (PSR).

  • Proliferative vitreoretinopathy (PVR).

  • Retinal vein occlusion (RVO).

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.


The patient often will report a sudden onset of either a single or multiple floating spots, along with flashing lights (photopsia). Visual symptoms will be stable within the patient's visual field. There may be precipitating ocular or head trauma. If there is a posterior vitreous detachment (PVD), there will also be one large floater. If there has been a vitreous hemorrhage, there will be multiple floaters. There may be a severe loss of vision if there is a dense vitreous hemorrhage or rhegmatogenous retinal detachment. However, in a number of cases, the patient is either asymptomatic or experienced symptoms so long ago that they were forgotten.


    The detachment has a concave configuration.

  • The subretinal fluid is shallower than in RRD and often does not extend to the ora serrata (the serrated extremity of the optic part of the retina, located a little behind the ciliary body and marking the limits of the percipient portion of the membrane).

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

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


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


The standard management of tractional retinal detachment has always been prophylactic laser photocoagulation or cryoretinopexy. This creates an RPE hyperplastic scar around the break and seals the retina to the RPE, thus preventing the accumulation of subretinal fluid and subsequent rhegmatogenous retinal detachment. However, not all cases benefit from prophylactic treatment. If the patient is aphakic or pseudophakic, has a history of previous retinal detachment in either eye, is about to undergo ocular surgery, or if the tear is fresh or associated with any hemorrhage, then the patient should receive prophylactic therapy.

If the patient is symptomatic with photopsia, or if there is more than one disc diameter of subretinal fluid or elevation extending beyond the edge of the break, the patient needs treatment, as the risk of detachment is high. Any tractional tears along the edge of lattice lesions also require treatment. If there are none of the above risk factors, the patient is asymptomatic and there is no subretinal fluid, monitor the patient on a six-week, three-month, six-month, 12-month schedule. If you see progression at any follow up visit, have the patient receive prophylactic treatment.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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