Retinal Detachment, Tractional 

  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 18, 2010
 

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).

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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.

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 compPatient 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 rhegThis 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.[4]

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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.

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Contributor Information and Disclosures
Author

Lihteh Wu, MD  Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica

Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Pan-American Association of Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Coauthor(s)

Teodoro Evans, MD  Retina Fellow, St Michael's Hospital, University of Toronto, Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

V Al Pakalnis, MD, PhD  Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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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 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 complicated by a tractional retinal detachment over the supertemporal arcade.
 
 
 
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