Signs and Symptoms

Tractional retinal tears (TRT) have no specific racial, gender or laterality predilection; rather, they are produced by complications of other pathologies which induce preretinal tension.1-32 Retinal tears are more common in the older population.

Tractional retinal tears are associated with posterior vitreous detachment (PVD), myopia with staphylomatous retinal stretching and vitreoretinal tension created by vitreoretinal interface abnormalities such as white with and without pressure, degenerative retinoschisis, cystic retinal tufts, epiretinal membrane, vitreomacular traction syndrome and rarely, zonular traction tufts on or near the border of lattice degeneration.7-10,13-16,32 Other vitreoretinal pathologies including Wagner’s syndrome and Stickler’s syndrome increase the risk of TRT.19

While intraretinal neovascular diseases such as proliferative diabetic retinopathy, ischemic venous occlusion and proliferative sickle-cell retinopathy can induce fibrovascular traction—which create retinal tears and tractional retinal detachment (TRD)—the typical cause is robust interaction of the vitreous along the border of vitreoretinal adhesion.1-30 In one study, the incidence of TRT in eyes with a symptomatic posterior vitreous detachment (PVD) was 8.2%.31 TRT are also associated with systemic diseases such as Marfan’s syndrome, Ehlers-Danlos syndrome and homocystinuria.19 Tractional retinal tears may lead to rhegmatogenous retinal detachment (RRD).1-25

Patients with TRT often report a sudden onset of either a single or multiple floating spots, along with flashing lights (photopsia).10-12 Unlike entoptic phenomena, which demonstrate exacerbations and remissions, or the scintillating scotoma produced in vasospastic events, the visual symptoms remain stable in the patient’s visual field.10-12 Pain is not a feature of any retinal detachment as the tissue has no pain receptors. There may be precipitating ocular or head trauma. If there has been a vitreous hemorrhage, there will be multiple large floaters or opacities which may take the form of “cobwebs.”10-12 There may be severe loss of vision if dense vitreous hemorrhage interrupts the visual axis or if a resultant RRD involves the macula. It is also possible that the patient is asymptomatic and unaware anything has occurred.12 The blood or retinal pigment epithelium (RPE) debris released from a TRT can be observed by the clinician during fundus examination and should be noted as “tobacco dust” or “Schaffer’s sign.”29


Retinal breaks are defined as full-thickness defects in the neurosensory retina.1,2,7-10,11,19 They typically occur anterior to the equator. All retinal detachments involve a dissection of the neurosensory retina from its underlying RPE layer by subretinal fluid (SRF).4,5 The principle involved in RRD is that forces exerted by the vitreous at the site of their attachment to the retina overcome its tensile strength, creating a full-thickness discontinuity through which fluid can migrate, separating the neurosensory retina from the underlying RPE.3,5,13,14,19

TRT often assume one of three forms: the flap tear (horseshoe-shaped tear), a retinal tear adjacent to an area of lattice degeneration or an operculated tear.1,2,4,14-19 The incidence of RRD without retinal breaks in the general phakic population is typically low (12/100,000).1-4,7,8,19 The natural prevalence of RRD increases to 14% with myopia greater than -3D; however, the risk increases dramatically when a symptomatic TRT is present.18,20 Byer notes that while the incidence of RRD from retinal breaks associated with lattice degeneration is low (0.3-0.5%), lattice degeneration may be associated with up to 60% of RRD.18 This is due to lattice degeneration being quite common and RRD uncommon in the general population.

The most common natural inciting process creating a TRT is posterior vitreous detachment.19-24 The vitreous “gel” is formed by a meshwork of collagen fibrils that provide a scaffold-like structure formed by hyaluronic acid.10 Firm attachments of the vitreous to the retina occur via chemical bonds through laminin, fibronectin and sulfated proteoglycans.10 The areas of firm adhesion include the vitreous base, the margin of the optic disc, the back of the crystalline lens (hyloidocapsular ligament of Wieger), the fovea, along large retinal vessels and sites of abnormal vitreoretinal anatomy such as the margins surrounding lattice degeneration.10,13,32,33 PVD begins with synchysis (vitreous liquefaction). This weakens the vitreoretinal adhesions.10 As the vitreoretinal adhesions dissolve, discontinuities form within the posterior hyaloid (either via fissure evolution or via a microbreak in the thin cortical vitreous layer).22 This allows liquid vitreous to enter the subhyaloid space dissecting the posterior hyaloid from the ILM.1,11,20-23

An anomalous PVD results when synchysis occurs without complete detachment from the ILM.27 This results in tractional effects at the interface.1,1120-23,32,33 The physics of PVD has the potential to generate forces which split the posterior vitreous cortex, causing vitreoschisis.10 When this phenomenon occurs, tractional forces increase the risk of TRT and RRD, especially at the margins of anatomically thin retina (lattice degeneration).1,13,32,33 The classic work of Foos identifies the pathogenic principles of TRT to include association with three topographical relationships to the vitreous base: intrabasal (caused by avulsion of zonular traction tufts) juxtabasal (related to traction of the posteriorly detached vitreous on irregularities in posterior border of vitreous base) and extrabasal (resulting from avulsion of cystic retinal tufts).32

Traumatic retinal breaks are theorized to result from rapid globe distortion with expansion and contraction. Here, vitreoretinal traction at the ora serrata and equator induces TRT, irregular breaks or retinal dialysis (circumferential breaks).19,26,27 Traumatic retinal breaks are documented to have an increased incidence in the inferotemporal and superonasal regions.19,27,28

Horseshoe-shaped tractional tears are triangular in appearance. The apex of the tear (posterior edge) may remain attached to mobile vitreous and points towards the posterior pole.1,19 The base of the tear is anchored at the vitreous base. Mechanical traction of mobile vitreous to the retina may enlarge the tear and physically separate it from the RPE creating “tobacco dust.”1,19,30 If the tear bridges a blood vessel, there can be subsequent vitreous hemorrhage.16 If an area of retinal tissue is pulled completely free and is observed to be floating in the vitreous, the lesion is considered an operculated tear with the free retinal tissue, termed the operculum.19 Operculated tears often signal complete vitreoretinal traction release.19

Classic evidence suggests that the edges of retinal breaks are covered by smooth cellular membranes, merging peripherally with a meshwork of vitreous fibrils.16 These membrane cells have poorly defined borders, a pitted surface and a variable number of microvilli.16 Lattice surfaces and paravascular retinal degenerations seem to be covered by similar membranes with subtle microscopic differences.16


The management of a TRT (observation vs. protective intervention) depends upon whether the risks of treatment outweigh the risks of retinal detachment.1,2,15,19,30 Tear location (superotemporal), size (larger TRT increase risk), symptoms (number one consideration), history of retinal detachment in the same eye or fellow eye, history of retinal detachment in the family, lifestyle (active vs. sedentary), the presence of myopia (greater than six diopters), the patient’s phakic status (phakic, pseudophakia, aphakia) and planned cataract surgery are all important factors.1,2,15,19,30

One study reported the rate of retinal detachment in symptomatic phakic patients with TRT to be 35%, strongly recommending prophylactic treatment for any break presenting in a patient complaining of flashing lights.19,34 Symptomatology in the form of photopsia is long held as the most important criterion for therapeutic intervention to reduce the risk of RRD.15,19 The modalities used to create the protective barrier around TRT, preventing subretinal fluid (SRF) infiltration and subsequent RRD, are cryoretinopexy and barrier laser photocoagulation.19,30

Cryoretinopexy involves transconjunctival cold application to create a seal between the chorioretinal tissues by destroying choriocapillaris, RPE and outer retinal elements and inducing retinal pigment epithelial hyperplasia.19,30-35 The hyperplastic RPE invades the sensory retina and creates a seal which makes migration of subretinal fluid and detachment of the retina difficult. The procedure requires three weeks for the seal to mature mandating reevaluation in that time period.19,30-33 Barrier laser photocoagulation uses argon blue-green, krypton red or diode delivery systems to create the same effect. Evidence suggests significant effects occur immediately with the maximal effect occurring in 10 days.19,30-35

Clinical Pearls

Tractional tears without symptoms or other risk factors may be safely monitored without treatment. However, a consult is advised.

The retinal pigment epithelium often becomes hyperplastic following an insult that produces a retinal tear. This chorioretinal scar may act as a natural seal around the break. When this happens, there is a lower risk of tractional/rhegmatogenous detachment.

In lightly pigmented fundi, natural RPE hyperplasia often does not occur. Additionally, cryoretinopexy and laser photocoagulation may be less effective.

Since eyes with a symptomatic posterior vitreous detachment develop retinal breaks in 8.2% of cases, patients presenting with new onset PVD with symptoms should be advised to limit strenuous activity and contact sports for a period of 3-6 weeks following the event. These patients should be re-examined with dilation and indirect ophthalmoscopy within 2-5 weeks of the initial presentation to confirm stable anatomy. Of course, patients developing increased floaters and flashes should be re-examined immediately. Patients with no increase in symptoms are highly unlikely to have any late retinal complications.

Asymptomatic atrophic retinal holes in lattice rarely lead to RRD and do not need prophylactic treatment.

Evidence suggests cases of TRT exhibiting vitreous hemorrhage should be considered for early vitrectomy.

1. Wilkinson CP. Rhegmatogenous retinal detachment. In: Yanoff M, Duker JS. Ophtalmology 2nd Ed. Mosby, Philadelphia, 2004: 982-989.

2. Haimann MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol. 1982;100(2):289-92.

3. Saika S, Yamanaka O, Okada Y, et al. TGF beta in fibroproliferative diseases in the eye. Front Biosci (Schol Ed). 2009;1(6):376-90.

4. Mitry D, Fleck BW, Wright AF, Campbell H, et al. Pathogenesis of rhegmatogenous retinal detachment: predisposing anatomy and cell biology. Retina. 2010;30(10):1561-72.

5. Müller B, Joussen AM. Myopic traction maculopathy – vitreoretinal traction syndrome in high myopic eyes and posterior staphyloma. Klin Monbl Augenheilkd. 2011;228(9):771-9.

6. Carrero JL. Incomplete posterior vitreous detachment: prevalence and clinical relevance. Am J Ophthalmol. 2012;153(3):497-503.

7. Lewis H. Peripheral retinal degenerations and the risk of retinal detachment. Am J Ophthalmol. 2003;136(1):155-60.

8. Byer NE. Lattice degeneration of the retina. Surv Ophthalmol.1979;23(4):213-48.

9. Iandiev I, Bringmann A, Wiedemann P. Proliferative vitreoretinopathy–pathogenesis and therapy. Klin Monbl Augenheilkd. 2010;227(3):168-74.

10. Hollands H, Johnson D, Brox AC, et al. Acute-onset floaters and flashes: is this patient at risk for retinal detachment? JAMA. 2009;302(20):2243-9.

11. Schweitzer KD, Eneh AA, Hurst J, et al. Predicting retinal tears in posterior vitreous detachment. Can J Ophthalmol. 2011;46(6):481-5.

12. Brda D, Tang EC. Visual hallucinations from retinal detachment misdiagnosed as psychosis. J Psychiatr Pract. 2011;17(2):133-6.

13. Wylegała E, Woyna-Orlewicz A, Piłat J, et al. Traction maculopathies–pathogenesis and diagnostics. Klin Oczna. 2006;108(10-12):457-63.

14. Byer NE. Cystic retinal tufts and their relationship to retinal detachment. Arch Ophthalmol. 1981;99(10):1788-90.

15. Byer NE. The natural history of asymptomatic retinal breaks. Ophthalmology. 1982;89(9):1033-9.

16. Robinson MR, Streeten BW. The surface morphology of retinal breaks and lattice retinal degeneration. A scanning electron microscopic study. Ophthalmology. 1986;93(2):237-46.

17. Burton TC. The influence of refractive error and lattice degeneration on the incidence of retinal detachment. Trans Am Ophthalmol Soc 1989;87(1):143–55.

18. Byer NE. Changes in and prognosis of lattice degeneration of the retina. Trans Am Acad Ophthalmol Otolaryngol 1974;78(1):114–25.

19. Greven CM. Retinal breaks. In: Yanoff M, Duker JS. Ophtalmology 2nd Ed. Mosby, Philadelphia, 2004: 978-81.

20. Skeie JM, Mahaian VB. Dissection of the human vitreous body elements for proteomic analysis. J Vis Exp. 2011:23(47)2455-64.

21. Sebag J. Age-related changes in human vitreous structure. Graefes Arch Clin Exp Ophthalmol. 1987;225(2):89-93.

22. Smiddy WE, Michels RG, Greene WR. Morphology, pathology, and surgery for idiopathic macular disorders. Retina. 1990;10(1):288–96.

23. Majcher CE, Gurwood AS. The role of the vitreous in retinal disease. Review of Optometry Retinal Supplement 2012; 149(4): 6s-14s.

24. Bottós J, Elizalde J, Arevalo JF, et al. Vitreomacular traction syndrome. J Ophthalmic Vis Res. 2012;7(2):148-61.

25. Schubert H, Kincaid M, Green R, et al. Anatomy and physiology. In: Regillo C, Brown G, Flynn H. Vitreoretinal disease: the essentials. New York, Thieme, 1999: 3-25.

26. Snead DR, James S, Snead MP. Pathological changes in the vitreoretinal junction 1: epiretinal membrane formation. Eye (Lond). 2008;22(10):1310-7.

27. Hagler WS, North AW. Retinal Dialyses and Retinal Detachment Arch Ophthalmol. 1968;79(4):376-388.

28. Hagler WS. Retinal dialysis: a statistical and genetic study to determine pathogenic factors. Trans Am Ophthalmol Soc. 1980;78(6):686-733.

29. Tanner V, Harle D, Tan J, et al. Original Article – Clinical science: Acute posterior vitreous detachment: the predictive value of vitreous pigment and symptomatology. Br J Ophthalmol 2000;84(11):1264-1268.

30. Wilkinson CP. Evidence-based analysis of prophylactic treatment of asymptomatic retinal breaks and lattice degeneration. Ophthalmology. 2000;107(1):12-5.

31. Coffee RE, Westfall AC, Davis GH, et al. Symptomatic posterior vitreous detachment and the incidence of delayed retinal breaks: case series and meta-analysis. Am J Ophthalmol. 2007;144(3):409-13.

32. Foos RY. Tears of the peripheral retina; pathogenesis, incidence and classification in autopsy eyes. Mod Probl Ophthalmol. 1975;15(1):68-81.

33. Spencer LM, Foos RY. Paravascular vitreoretinal attachments. Role in retinal tears. Arch Ophthalmol. 1970;84(5):557-64.

34. Davis MD. Natural history of retinal breaks without detachment. Arch Ophthalmol. 1974;92(3):183-94.

35. Framme C, Roider J, Brinkmann R, et al. Basic principles and clinical application of retinal laser therapy. Klin Monbl Augenheilkd. 2008;225(4):259-68.