Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

.pdf
Скачиваний:
0
Добавлен:
28.03.2026
Размер:
44.2 Mб
Скачать

21.Whitcup, S., Csaky, K., Podgor, M., et al. A randomized, masked, cross-over trial of acetazolamide for cystoid macular edema in patients with uveitis. Ophthalmology 1996; 103: 1054.

22.Melberg, N., Olk, J. Corticosteroid-induced ocular hypertension in the treatment of aphakic or pseudophakic cystoid macular edema. Ophthalmology 1993; 100: 164.

23.Matthew A. Cunnigham, Jeffrey L. Edelman, Shalesch Kaushal, et al. Intravitreal Steroids for Macular Edema: The Past, the Present and the Future. Survey Ophthalmology 2008. 53; 2: 139–149.

24.Baruch D. Kuppermann, Mark S. Blumenkranz, et al. Randomized Controlled Study of an Intravitreous Dexamethasone Drug Delivery System in Patients with Persistent Macular Edema. Arch Ophthalmol 2007; 125: 309–317.

25.Nathanael Benhamou, Pascale Massin, Belkacem Haouchine, et al. Intravitreal Triamcinolone for Refractory Pseudophakic Macular Edema.Am J Ophthalmol 2003;

135:246–249.

26.Barone, A., Francesco Prascina, Vincenzo Russo, et al. Successful treatment of pseudophakic cystoid macular edemawithintravitrealbevacizumab.JCataractRefract Surg 2008. 34; 7: 1210–1212.

27.Martin S. Spitzer, Focke Ziemssen, Efdal Yoeruek, et al. Efficacy of intravitreal bevacizumab in treating postoperative pseudophakic cystoid macular edema. J Cataract Refract Surg 2008. 34: 70–75.

28.Wu L, Martinez-Castellanos MA, Quiroz-Mercado H, et al. Twelve month safety of intravitreal injections of bevacizumab (Avastin®): results of the Pan American Collaborative Retina Study Group (PACORES). Arch Clin Exp Ophthalmol 2007 Aug 3; [Epub ahead of print]

Cystoid Macular Edema

343

29.Arevalo, J., Garcia-Amaris, Roca, J., Wu, L., et al. Primary intravitreal bevacizumab for the management of pseudophakic cystoid macular edema: Pilot study of the Pan-American Collaborative Retina Study Group. J Cataract Refract Surg 2007. 33; 12: 2098–2105.

30.Fung, W. Vitrectomy ACME Study Group. Vitrectomy for chronic aphakic cystoid macular edema. Results of national, collaborative, prospective, randomized investigation. Ophthalmology 1985; 92: 1102.

31.Harbour, W., Smiddy, W., Rubsamen, P., et al. Pars plana vitrectomy for chronic pseudophakic cystoid macular edema. Am J Ophthalmol 1995; 120: 302.

32.Federman, J., Annesley, W., Sarin, L., et al. Vitrectomy and cystoid macular edema. Am J Ophthalmol 1980;

87:622.

33.Pendergast, S., Margherio, R., Williams, G., et al. Vitrectomy for chronic pseudophakic cystoid macular edema. Am J Ophthalmol 1999. 128: 3; 317–323.

34.Ehab Abdelkader, Noemi Lois. Internal Limiting Membrane Peeling in Vitreo-retinal Surgery. Surv Ophthalmol 2008; 53: 368–396.

35.Gholam, A., Christina Canakis, et al. The Effect of Internal Limiting Membrane Peeling on Chronic Recalcitrant Pseudophakic Cystoid Macular Edema: A Report of Two Cases. Am J Ophthalmol 2002; 133: 571–572.

22

Traction Maculopathies:

Vitreomacular Traction

Syndrome, Cellophane

Maculopathy, Macular

Pucker, Macular Hole

Ferenc Kuhn, MD, Ph.D.,

Robert Morris, MD,

C. Douglas Witherspoon, MD, FACS

Introduction

Traction can be defined as a synonym for force. On the macula, this force can manifest in two vectors: anteroposterior (i.e., originating in the vitreous body) or tangential (i.e., forming on the retinal surface; Figures 1A, 1B). (Author's Note: Traction force can also be created by subretinal scarring; this entity is not discussed here.) The resulting anatomical changes (retinal distortion, fold formation, vascular leakage etc.) can quickly lead to functional consequences in most cases; how early the patient seeks ophthalmologic consultation, though, shows great variability, due to the normal fellow eye’s dominance as well as to the individual’s personality and visual needs.

Vascular incompetence due to traction can occur as reflected in the abnormal fluorescein angiogram. Due to chronic traction-related

vascular incompetence, the macular tissue may become diffusely edematous. The fovea can develop cystic changes over time, which are usually reversible after traction release if the intervention is timely. In extreme cases, however,theuntreatedfovealcystscandevelop into partialor full-thickness holes. Longstanding traction can also produce separation (i.e., true detachment) of the neuroretina in an area involving the fovea or macula.

The cause of traction development is usually unknown (idiopathic); occasionally, the etiology is identifiable: trauma, inflammation, proliferative vitreoretinopathy, etc.

Classification

The term (coined by Robert Morris, MD) “traction maculopathy”1 encompasses four distinct conditions and its common pathogenesis (see Table 1).

Retinal andVitreoretinal Diseases and Surgery

346

Figure 1A: Epimacular proliferation (EMP) before contraction (rope men). Glial cells (G), internal limiting membrane (I), retina

(R). (Art from Jaypee - Highlights Medical Publishers).

Figure 1B: Epimacular proliferation (EMP) after contraction (rope men). Internal limiting membrane (I), retina (R).

(Art from Jaypee - Highlights Medical Publishers).

Traction Maculopathies

347

Table 1

The Classification of Traction Maculopathies

 

Name of Condition

Traction Force

Retinal Effect

 

 

 

 

 

Vitreomacular traction

Anteroposterior

Full-thickness

 

syndrome

 

 

 

 

 

 

 

 

 

Cellophane

maculopathy

Tangential

Surface

 

 

 

 

 

 

Epimacular

proliferation

Tangential

Partial-thickness

 

(macular

pucker)

 

(inner retina)

 

 

 

 

 

to full-thickness

 

 

 

 

 

 

Macular

hole

Anteroposterior and

Full-thickness

 

 

 

 

tangential

 

 

 

 

 

 

 

Diagnostics

History. Although the condition may be a serendipitous finding, in most cases it is the patient who discovers the functional disturbance. A long history is important because it typically interferes with good visual recovery.

Visual function. A deterioration of visual acuity is the most common finding (and complaint given by the patient), but upon careful testing (and questioning), a distortion of vision is just as often found (hence the recommendation, in addition to the standard visual acuity testing, to utilize the Amsler grid, which shows deformation centrally). (Author's Note: The Amsler grid is a very effective initial diagnostic tool, but it is ineffective to detect further deterioration. The

human brain remembers the previously seen image and does not appreciate the subsequently shown image as new (false-negative test result). The reading speed is another valuable test: A significant drop in the speed of reading a standardized text (MNREAD) may be demonstrated. (Author's Note: This is a crucial advantage over the standard visual acuity testing: the latter measures the reading of single letters, as opposed to the closer-to-life situation of measuring reading ability with the MNREAD test).

Slit lamp biomicroscopy with a 90 D or, preferably, a contact lens. This is the most useful easily available diagnostic tool, allowing the ophthalmologist to view not only the macula in great detail (Figure 2) but also the certain vitreous pathologies (e.g., the presence anteroposterior traction if significant).

Retinal andVitreoretinal Diseases and Surgery

348

Figure 2: Funduscopic image of an epimacular proliferation. A distinct membrane in the macula as well as marked distortion of the blood vessels around the fovea can clearly be delineated. Fine retinal folding is also visible. (Image courtesy of Viktoria Mester, MD.)

Binocular ophthalmoscopy. Although giving fewer fine details than obtainable at the slit lamp, the binocular ophthalmoscope is of great value to show the entire vitreous cavity and widespread vitreoretinal pathologies. (Author's Note: i.e., seeing the “forest, not only the trees”). Foveal ectopia, which can cause diplopia, is easier to detect when one sees the entire posterior pole, not just a smaller central area of the retina, and compares this image with the fundus of the fellow eye.

Optical coherence tomography (OCT). This relatively new but rapidly evolving diagnostic modality is becoming the major weapon in the ophthalmologist’s armamentarium to not only diagnose lesions that may be invisible otherwise (Figure 3A), but also to follow the macula over time as a noninvasive procedure (Figure 3B). The test is thus ever more commonly utilized for diagnosis as well as for following anatomical changes occurring spontaneously (natural history) or after surgery.

Traction Maculopathies

349

A

Figure 3A-B: The clinical benefits of

B

OTC imaging. A) OCT image of an

 

eye with a partially detached poste-

 

rior vitreous face, a partial-thickness

 

macula hole, and intraretinal cysts. B)

 

The same eye with a normal macular

 

architecture 3 months postoperatively.

 

(ImagescourtesyofViktoriaMester,MD.)

 

 

 

Fluorescein angiography. Although it is an invasive diagnostic tool, it is still the only method to show vascular leakage (Figures 4A and B).

Electrophysiology. The multifocal electroretinogram shows marked central depression in eyes with foveal dysfunction (Figure 5); the test is uncommonly utilized in clinical practice but is a good method to follow macular function changes following surgery.

Counseling

Once the diagnosis has been established, it is the ophthalmologist’s responsibility to explain the condition to the patient. The ophthalmologist must describe the natural history – typically one of continual dete-

rioration, although of variable speed -, and the benefits as well as risks of surgery, giving specific numbers (percentages) if these are available. In an ideal situation, it is the patient who chooses to undergo treatment, not the ophthalmologist. (Author's Note: It is unacceptable for the ophthalmologist to set an arbitrary limit below which he would refuse to undertake surgery. It is often said by these ophthalmologists that “I will not operate on a macular hole unless vision is 20/40 or worse”; such – scientifically unjustified – statements do not take into consideration that one individual’s needs and desires can greatly differ from another person’s. Surgery is not done on a macular hole but on an individual who has a macular hole).

The patient must understand that even if the visual symptoms are minimal, certain

Retinal andVitreoretinal Diseases and Surgery

350

A B

Figure 4 A-B: Macular Pucker fluorescein angiogram. A) Extensive fluorescein leakage from retinal blood vessels in the late phase, secondary to traction forces of epimacular proliferation, preoperative. B) Macular pucker fluorescein angiogram, postoperative. Fluorescein leakage has now largely resolved six weeks after removal of all epimacular proliferation.

A

 

B

 

 

 

Figure 5 A-B: A) Multifocal Electroretinogram (MFERG), normal. Note the high peak at the foveola, with gradual taper in the surrounding foveal and macular tissue. B) Multifocal Electroretinogram (MFERG), abnormal, macular pucker. Note the severely depressed central peak corresponding with foveal dysfunction secondary to EMP traction.

Traction Maculopathies

351

complications of traction maculopathy, such as cystoid edema, may cause damage that can prove irreversible if the intervention is delayed indefinitely.

Treatment

The only predictable and effective method to treat patients with traction maculopathy is pars plana vitrectomy. Until a few years ago, all operations would have been performed using 20 g systems, but today many surgeons elect to use smaller g instrumentation (23 or 25 g). (Author's Note: Technical details related to gauge are not discussed in this chapter). In addition, when using the term “complete vitrectomy” here, it rarely means that a radical peripheral vitrectomy with scleral indentation is done; rather, the vitreous base is left intact in most eyes.

For further details, see the individual conditions described below.

Vitreomacular Traction Syndrome

Figure 6: Vitreomacular Traction Syndrome. The top view shows how the vitreous (V) may exert anterior posterior traction (arrow) on the macula (M) as a consequence of forward movement of the vitreous coupled with persistent attachment of cortical vitreous at the macula. Below shows the focally intensified forces (arrows) of the vitreous traction on the macula (M) as exerted by the mass of the entire body of the free moving vitreous.

Dependingontheseverity of the condition, the patient may notice a distinct drop in visual acuity or a severe drop as well as mild to significant distortion(metamorphopsia). An incomplete detachment of the posterior hyaloid face (PHF) is the cause (Figures 6 and 7), but the vitreous may also be completely attached with firm connection to the

internal limiting membrane (ILM), pulling on it as the degenerating vitreous moves. Epimacular proliferation may also be present.

Figure 7: OCT imaging of vitreomacular traction syndrome. The partially detached posterior vitreous face shows strong adhesion to the retina centrally (arrows), causing a dramatic change in the macular contour.

(Image courtesy of Viktoria Mester, MD.)

Retinal andVitreoretinal Diseases and Surgery

352

The OCT may show the actual PHF as well as its attachment to the retina.

Treatment: Removal of the entire vitreous, especially posteriorly (see below in more detail). This is greatly aided by the use of triamcinolone acetonide (TA) as a marker to show the vitreous that otherwise would remain invisible. It is highly recommended to remove the ILM as well, both to make sure that no vitreous is left behind and also because the ILM may also be pathological.

It is helpful to stain the ILM before removal; this makes the procedure less traumatic to the retina, less stressful to the surgeon, and not only reduces the time needed for removal but also allows it to be more complete (see below for details).

The surgeon should consider indirect oph- thalmoscope-delivered encircling laser prophylaxis (Figure 8) to almost eliminate the major risk of vitrectomy for traction maculopathy: retinal detachment from a peripheral break.

Prognosis: If surgery has been timely, excellent outcome is expected; if, however, the condition has been present for an extended period of time and the vision is severely affected, the functional result will not match the anatomical one. The patient must be made aware of this during counseling (see above).

Cellophane Maculopathy

Figure 8: Indirect Ophthalmoscope (IDO) Laser Cerclage Prophylaxis.

is a mild variation of an epimacular proliferation but still interpreted as a distinct entity since no membrane is visible on the retinal surface. With the retinal traction involving only the superficial retina (Figures 9 and 10, this condition can be interpreted as a mild form of an epimacular proliferation. There is no visible membrane present (it is also possible that it is just too thin for detection with current technology), but cells seeding the surface do cause anatomically visible changes. Careful examination is necessary to detect the fine “wave formation” of the retinal surface; often this is best seen intraoperatively, once the retina has been stained. Of the four conditions mentioned herein, this is the least urgently in need of treatment.

(Authoŕs Note: “Preretinal gliosis” is another term occasionally, but incorrectly, used. As described above, cellophane maculopathy

Treatment: If the patient is sufficiently bothered by the metamorphopsia caused by contracted ILM (resembling wrinkled