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Chapter 130 – Vitreomacular Traction Syndrome

Chapter 130 – Vitreomacular Traction Syndrome

 

WILLIAM E. SMIDDY

 

 

 

 

 

DEFINITION

• Incomplete posterior vitreous separation with preretinal tissue proliferation and associated macular traction distributed in the zone of persistent vitreous attachment.

 

KEY FEATURES

• Prominent vitreoretinal attachment at the posterior pole.

• Peripheral vitreous detachment.

• Epiretinal membrane proliferation.

 

ASSOCIATED FEATURES

• Distortion of the internal limiting membrane with retinal striae and vascular tortuosity.

• Macular edema.

• Localized traction-related macular retinal detachment.

• Retinal vascular and optic disc staining on fluorescein angiography.

 

 

 

INTRODUCTION

The effects of vitreous-induced traction on the neural retina are dependent upon the site, extent, and cause of the traction. Anterior vitreoretinal traction may induce peripheral retinal breaks and lead to retinal detachment.[1] Vitreoretinal traction at the macula may induce a broad range of effects, including retinoschisis, cystoid macular edema, and preretinal traction effects. [2] [3] [4] [5] [6] [7] [8] Although debated, vitreomacular traction may be the initiating cause of macular hole formation.[7] [9] [10]

Macular traction induced by preretinal tissue of a typical macular pucker most commonly is associated with complete posterior vitreous detachment. Vitreomacular traction syndrome has been differentiated from idiopathic macular pucker by virtue of the association of the preretinal tissue with persistent vitreomacular attachment. [1] Persistent vitreomacular attachment may assume a multiplicity of configurations. Ophthalmoscopically, the condition commonly mimics idiopathic macular pucker or macular hole syndromes, but specific clinical, angiographic, ultrasonographic, prognostic, and intraoperative features distinguish it. These factors should be recognized by the physician to deliver optimal management.

EPIDEMIOLOGY AND PATHOGENESIS

Vitreomacular traction syndrome was described first by Reese et al., both clinically[11] and histopathologically,[12] as a condition characterized by persistent vitreous attachment in the center of the macula, causing a cystoid configuration and decreased vision. More commonly described is broad-based vitreoretinal attachments. [13] [14] [15] [16] [17] [18] Jaffe[13] [14] described several cases; most resolved spontaneously as completion of a posterior vitreous detachment was observed. These probably represent mild cases in a clinical

 

 

Figure 130-1 Schematic representation of vitreomacular traction syndrome which depicts the peripheral posterior vitreous separation (arrows) and vitreomacular attachment in the zone that involves the macula. It is uncertain whether the macular traction impedes completion of the posterior vitreous separation or whether the aborted posterior vitreous separation stimulates preretinal tissue proliferation.

spectrum, with delayed posterior separation of an unusually prominent posterior vitreous surface. Others have described cases with vitreomacular traction features in the class of macular hole precursors,[7] while still others include this entity in idiopathic macular pucker cases.[19] Rarely, preretinal membranes may peel spontaneously, [20] [21] [22] [23] a sequence that may be mimicked by or possibly represented by vitreomacular traction syndrome if the persistent posterior vitreous attachment releases, as apparently occurred in many of Jaffe’s cases.

No known racial predilection exists for vitreomacular traction syndrome. Most reported studies include about 65% women. [12] [13] [14] [15] [16] [17] [18] The reported age range is 26–85 years, but most patients are in their sixth or seventh decade.

The pathogenesis of vitreomacular traction syndrome is unknown. Possibly, the unusually firm posterior hyaloid attachment stimulates cell proliferation. Alternatively, primary preretinal tissue proliferation may limit the normal process of posterior vitreous separation ( Fig. 130-1 ).

OCULAR MANIFESTATIONS

The typical clinical picture of a patient who has vitreomacular traction syndrome involves decreased central vision with some degree of metamorphopsia ( Fig. 130-2 ). Even patients who have 20/20 (6/6) vision may manifest fairly extensive preretinal tissue and moderate symptoms. Symptoms usually develop over several weeks and patients seek treatment after persistence of such

 

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Figure 130-2 A 71-year-old man with a 1-month history of decreased vision in the left eye to 20/80 (6/26). The vision in the right eye was 20/40 (6/13) with an preretinal membrane and pseudohole configuration. A, Clinical appearance of the patient’s eye, with features of bilateral vitreomacular traction syndrome, left eye. Fluorescein angiogram preoperatively shows (B) early and (C) late cystoid pattern of leakage. D, The macular appearance is improved markedly 3 months following surgery for vitreomacular traction syndrome. After 2.5 years postoperatively (and after cataract extraction), vision was 20/25 (6/8) in the left eye. Typical features of fibrous astrocytes include a multilayered growth pattern with a base of membrane (arrowheads) and characteristic 10?mm diameter intracytoplasmic filaments. (From Greven GM, Slusher MM, Weaver RG. Epiretinal membrane release and posterior vitreous detachment. Ophthalmology. 1988;95:902–5.)

symptoms. On Watzke-Allen testing, patients may report “thinning” of the beam, without total central disappearance.[16]

In many patients, the disease will not progress and symptoms may remain fairly mild. A subset of patients progress from minimal to severe symptoms and disproportionately visit a retina specialist, usually with visual acuity of 20/50 (6/16) or worse. The natural history of such patients is usually continued slow progression of traction, with moderate cystoid macular edema changes, and visual loss stabilizing around the level of 20/200 (6/60). The hallmark of vitreomacular traction syndrome is persistent anterior-to-posterior traction on the macula, which usually is directly observable[24] (see Fig. 130-2, A ). Often, a segment of the attachment is visible as a curvilinear attachment site, but the entire perimeter of the attachment may not be visible. Indeed, entire peripheral quadrants of persistent vitreous attachment may be demonstrable intraoperatively but may be difficult to observe preoperatively by clinical examination.[17] The profile of the vitreous against the optically clear retrohyaloid space usually is most prominent immediately anterior to its attachment site. The zone of vitreoretinal attachment typically involves a region of several disc areas centered on the fovea and frequently extends nasally to encompass the optic nerve head.

Associated cystoid macular changes are present in up to 95% of cases.[17] In many cases, the cystoid spaces accumulate fluorescein dye on angiography (see Fig. 130-2, B and C ); this may mimic postoperative cystoid macular edema in pseudophakic eyes. The extent of premacular fibrous proliferation usually corresponds to the zone of macular vitreous attachment. Rarely, the traction is extreme enough to induce focal tractional retinal detachment and has been distinguished as a separate diagnostic entity.[25] [26]

DIAGNOSIS AND ANCILLARY TESTING

The diagnosis of the condition rests primarily on the observation of the preretinal tissue in association with the vitreomacular traction attachment, as described above. Fluorescein angiography may help to confirm the diagnosis by revealing dye leakage from the affected posterior pole vessels and, on occasion, from the optic disc. A “B” scan ultrasonic examination may demonstrate the peripheral detached posterior hyaloid with the attached hyaloid over the posterior pole, differentiating the vitreomacular traction syndrome from idiopathic macular pucker, in which a completely separated, mobile posterior vitreous surface is present ( Fig. 130-3, A ). Ocular coherence tomography (OCT) also demonstrates the pathognomonic vitreoretinal attachment ( Fig. 130-3, B ). [31]

DIFFERENTIAL DIAGNOSIS

Idiopathic macular pucker is the most commonly encountered condition that may mimic vitreomacular traction syndrome. With macular pucker, however, Weiss’ ring usually is present, which indicates complete posterior vitreous detachment. Stage 1 macular hole and lamellar macular holes also may mimic vitreomacular traction syndrome (see Fig. 130-2, B ) but, in these, neither the vitreomacular attachment nor the preretinal tissue is

 

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Figure 130-3 A, Ultrasonographic feature of patient who has vitreomacular traction syndrome. The insertion of vitreous into the posterior pole is demonstrated. B, A 67-year-old female with central metamorphopsia and visual loss to 20/200 has visible vitromacular insertion, causing macular distortion.

as prominent. Prominent internal limiting membrane stippling due to pseudophakic cystoid macular edema also may mimic the surface wrinkling appearance and, especially in the absence of posterior vitreous detachment, may resemble vitreomacular traction syndrome. Also, early stages of macular hole may mimic vitreomacular traction syndrome, but the risk of developing a full-thickness macular hole is extremely low in these patients (although it has been observed).

PATHOLOGY

The original case described by Reese et al. [12] was studied postmortem; vitreous attachment at the fovea and cystoid macular changes were found. A review of the electron microscopic features of the preretinal membrane tissue removed from eyes with vitreomacular traction syndrome showed a high prevalence of fibroglial tissue[27] ( Fig. 130-4 ). Retinal pigment epithelial cells were notably absent. This contrasts sharply to the retinal pigment epithelial cells that dominate idiopathic macular pucker specimens[28] and suggests a separate pathogenic mechanism. Also, thickened internal limiting lamina, astrocyte elements, and myofibrocytes have been identified in an electron microscopy and immunohistochemical study.[29] These findings bespeak a tighter vitreoretinal adhesion and may explain the clinical finding of petechial hemorrhages seen intraoperatively after removing the preretinal tissue component.

TREATMENT

Most cases do not require treatment. Patients often have relatively good visual acuity and only mild metamorphopsia, which

 

 

Figure 130-4 Histopathology of membrane specimen removed from a patient who has vitreomacular traction syndrome. Typical features of fibrous astrocytes include a multilayered growth pattern with a base of membrane (arrowheads) and characteristic 10?nm diameter intracytoplasmic filaments. (From Greven GM, Slusher MM, Weaver RG. Epiretinal membrane release and posterior vitreous detachment. Ophthalmology. 1988;95:902–5.)

usually remains stable. Some cases may resolve spontaneously, with completion of the posterior vitreous separation,[13] [14] [30] which has been demonstrated by OCT,[31] but this sequence is observed infrequently and a substantial proportion have progressive traction and visual loss.[32] Once the visual acuity drops to 20/60 (6/20) or worse, surgical treatment should be considered.

The surgical treatment involves three-port pars plana vitrectomy and utilizes standard vitreous surgical techniques [15] [16] [17] [18] [33] ( Fig. 130-5 ). Removal of anterior-to-posterior traction has been advocated with secondary removal of preretinal tissue. An edge is identified with a sharp needle or pick; a more generalized dissection is then made with a pick to elevate the preretinal tissue from the retinal surface, and ultimately removal is by intraocular forceps as for cases of macular pucker. An alternative strategy uses an en bloc approach, with initial release of the posterior vitreous attachment so as to utilize the support and stability that anterior-to-posterior vitreous orientation offers.[17]

A unique finding in the surgical anatomy is a “double layer” of preretinal proliferation in about 15% of cases. The anterior layer may represent simply a thickened posterior hyaloid. Deep to that on the internal surface of the neural retina, a second, preretinal layer may be found in up to 15% of cases.[17] In cases of macular pucker there is not a second layer, but opacities of the nerve fiber layer due to traction-induced axoplasmic stasis may mimic a second layer and should not be dissected.

COURSE AND OUTCOME

The results in the three reported series that involved surgical intervention are summarized in Table 130-1 .[15] [17] [18] [33] An additional reported series includes similar cases, but the data were not presented separately from other cases.[16] The preoperative visual acuity was <20/100 (6/33) in 60–78%, improved by at least two lines in 44–70%, and had a final visual acuity of >20/100 (6/30) in 44–80% of cases. The visual results are better with earlier surgical intervention.[33] Scanning laser ophthalmoscopic microperimetry studies have demonstrated a small central scotoma that resolves postoperatively.[34] The characteristic cystoid macular edema[26] has been demonstrated to resolve using ocular coherence tomography[35] [36] and fluorescein angiography,[37] as has the vitreomacular traction.

 

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Figure 130-5 Surgical features of vitreomacular traction syndrome. A, Removal of anterior-to-posterior traction by incision of the posterior hyaloid. B, Development of surgical plane for removal of preretinal membrane. C, Removal of preretinal tissue with forceps. (From Jaffe NS, ed. Atlas of ophthalmic surgery. St Louis: Mosby; 1996:209.)

 

 

TABLE 130-1 — SUMMARY OF SERIES OF VITREOMACULAR TRACTION SYNDROME

 

 

Percentage Width Visual Activity >20/100 (6/33)

 

 

Series

Number of Eyes

Preoperatively

Postoperatively

% >2 Lines

Complications

Smiddy et al.

16

63

69

63

MacDonald et al.

20

60

80

70

4 with breaks

Melberg et al.

9

78

44

44

1 with break; 1 postoperative retinal detachment

Data from Smiddy WE, Michels RG, Glaser BM, deBustros S. Vitrectomy for macular traction caused by incomplete vitreous separation. Arch Ophthalmol. 1988;106:624–8.

RD, Retinal detachment.

 

 

Surgical complication rates are expected to be similar to rates generally extrapolated from those for macular pucker, which include a postoperative retinal detachment rate of 5% or less and a high frequency of induced accelerated nuclear sclerosis. Only about 90 cases have been reported, so accurate data are not available, but acceptably low complication rates have been found. [15] [16] [17] [18] [33] Of note, however, is that the series with the en bloc technique had a slightly higher rate of intraoperative peripheral breaks, but all were successfully controlled with retinal cryopexy and fluid–gas exchange. [17]

 

 

REFERENCES

 

1. Green WR. Vitreoretinal juncture. In: Ryan SJ, ed. Retina. St Louis: Mosby; 1989:13–69.

 

2. Sebag J, Balazs EAC. Pathogenesis of cystoid macular edema: an anatomic consideration of vitreoretinal adhesions. Surv Ophthalmol. 1984;28:495–8.

 

3. Boniuk M. Cystoid macular edema secondary to vitreoretinal traction. Surv Ophthalmol. 1968;13:118–21.

 

4. Nasrallah FP, Jalkh AE, van Coppenolle F, et al. The role of the vitreous in diabetic macular edema. Ophthalmology. 1988;95:1335–9.

 

5. Lewis HL, Abrams GW, Blumenkranz MS, Campo RV. Vitrectomy for diabetic macular traction and edema associated with posterior hyaloid traction. Ophthalmology. 1992;99:753–9.

 

6. Michels RG. Macular pucker. In: Ryan SJ, ed. Retina. St Louis: Mosby; 1989:419–30.

 

7. Gass JDM. Vitreous traction maculopathy in stereoscopic atlas of macular diseases. St Louis: Mosby; 1987:678–83.

 

8. Falcone PM. Vitreomacular traction syndrome confused with pseudophakic cystoid macular edema. Ophthalmic Surg Lasers. 1996;27:392–4.

 

9. Gaudric A, Haouchine B, Massin P, et al. Macular hole formation. Arch Ophthalmol. 1999;117:744–51.

 

10. Kakehashi A, Schepens CL, Trempe CL. Vitreomacular observations. II. Data on the pathogenesis of idiopathic macular breaks. Graefes Arch Klin Exp Ophthalmol. 1996;234:425–33.

 

11. Reese AB, Jones IR, Cooper WC. Macular changes secondary to vitreous traction. Am J Ophthalmol. 1967;51:544–9.

 

12. Reese AB, Jones IR, Cooper WC. Vitreomacular traction syndrome confirmed histologically. Am J Ophthalmol. 1970;69:975–7.

 

13. Jaffe NS. Vitreous traction at the posterior pole of the fundus due to alterations in the vitreous posterior. Trans Am Acad Ophthalmol Otolaryngol. 1967;71:642–52.

 

14. Jaffe NS. Macular retinopathy after separation of vitreoretinal adherence. Arch Ophthalmol. 1967;78:585–91.

 

15. Smiddy WE, Michels RG, Glaser BM, deBustros S. Vitrectomy for macular traction caused by incomplete vitreous separation. Arch Ophthalmol. 1988;106:624–8.

 

16. Margherio RR, Trese MT, Margherio AR, Cartright K. Surgical management of vitreomacular traction syndromes. Ophthalmology. 1989;96:1437–45.

 

17. MacDonald HR, Johnson RN, Schatz H. Surgical results in the vitreomacular traction syndrome. Ophthalmology. 1994;101:1397–403.

 

18. Melberg N, Williams DF, Balles MW, et al. Vitrectomy for vitreomacular traction syndrome with macular detachment. Retina. 1995;15:192–7.

 

19. Hirokawa H, Jalk AE, Takahashi M, et al. Role of vitreous in independent preretinal macular fibrosis. Am J Ophthalmol. 1989;101:166–9.

 

20. Byer NE. Spontaneous disappearance of early postoperative preretinal traction. Arch Ophthalmol. 1973;90:133–5.

 

21. Messner KH. Spontaneous separation of preretinal macular fibrosis. Am J Ophthalmol. 1977;83:9–11.

 

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22. Sumers KD, Jampol LM, Goldberg MS, Huamonte FU. Spontaneous separation of epiretinal membranes. Arch Ophthalmol. 1980;98:318–20.

 

23. Greven GM, Slusher MM, Weaver RG. Epiretinal membrane release and posterior vitreous detachment. Ophthalmology. 1988;95:902–5.

 

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

 

25. Thomas EL, Michels RG, Rice TA, et al. Idiopathic progressive unilateral vitreous fibrosis and secondary traction retinal detachment. Retina. 1982;2:134–44.

 

26. Hashimoto E, Hirakata A, Hotta K, et al. Unusual macular retinal detachment associated with vitreomacular traction syndrome. Br J Ophthalmol. 1998;82:326–7.

 

27. Smiddy WE, Green WR, Michels RG, de la Cruz Z. Ultrastructural studies of vitreomacular traction syndrome. Am J Ophthalmol. 1989;107:177–85.

 

28. Smiddy WE, Maguire AM, Green WR, et al. Idiopathic epiretinal membranes. Ultrastructural characteristics in clinical pathologic correlation. Ophthalmology. 1989;96:811–21.

 

29. Shinoda K, Hirakata A, Hida T, et al. Ultrastructural and immunohistochemical findings in five patients with vitreomacular traction syndrome. Retina. 2000;20:289–93.

 

30. Kakehashi A, Schepens C, Akiba J, et al. Spontaneous resolution of foveal detachments and macular breaks. Am J Ophthalmol 1995;120:767–75.

 

31. Sulkes D, Ip M, Baumal C, et al. Spontaneous resolution of vitreomacular traction documented by optical coherence tomography. Arch Ophthalmol. 2000;118: 286–7.

 

32. Hikichi T, Yoshida A, Trempe C. Course of vitreomacular traction syndrome. Am J Ophthalmol. 1995;119:55–61.

 

33. Koerner F, Garweg J. Vitrectomy for macular pucker and vitreomacular traction syndrome. Doc Ophthalmol. 1999;97:449–58.

 

34. Goto M, Nishimura A, Shirao Y. Scanning laser ophthalmoscopic microperimetry on idiopathic epiretinal membrane and vitreomacular traction syndrome. Jpn J Ophthalmol. 2001;45:115.

 

35. Kusaka S, Saito Y, Okada A, et al. Optical coherence tomography in spontaneously resolving vitreomacular traction syndrome. Ophthalmologica. 2001;215:139–41.

 

36. Ito Y, Terasaki H, Mori M, et al. Three-dimensional optical coherence tomography of vitreomacular traction syndrome before and after vitrectomy. Retina. 2000;20:403–5.

 

37. Pournaras CJ, Kapetanios AD, Donati G. Vitrectomy for traction macular edema. Doc Ophthalmol. 1999;97:439–47.

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One comment on “Chapter 130 – Vitreomacular Traction Syndrome

  1. If you have been clinically determined to have macular destruction it is necessary that you will be discovering a good ophthalmologist who is specifically trained in retinal illnesses just like …

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