21 Retinal detachment and proliferative
Oh Woong Kwon, MD, PhD, Mi In Roh, MD, and Ji Hun Song, MD
RD occurs at a rate of 5–16 per 1000 cases following cataract surgery,
INTRODUCTION and this comprises approximately 30–40% of all reported RD.4 The
cumulative probability ratio of RD at 20 years after extracapsular cata-
Proliferative vitreoretinopathy (PVR) is a disease entity related to a ract extraction or phacoemulsiﬁcation is reported to be 1.58%, which is
number of intraocular diseases, including retinal detachment (RD). four times higher than for patients not undergoing cataract extraction.5
Several studies have conﬁrmed the hypothesis that PVR occurs as a The risk factors associated with RD in cataract removal are accidental
reparative process induced by retinal breaks and excessive inﬂamma- posterior capsule rupture at the time of surgery, young age, increased
tory reaction. A survey of recently published series suggested that the axial length, a deep anterior chamber, RD in the fellow eye, and male
frequency of PVR remains largely unchanged in primary RD, with the gender.6,7 While the incidence of RD after clear lens extraction in myopic
incidence ranging from 5.1 to 11.7%.1 PVR is the most common cause eyes rises to 8.1%, the incidence of RD decreases to 2.7% with the intro-
of failed repair of rhegmatogenous RD and risk factors for PVR are duction of small incision coaxial phacoemulsiﬁcation.8,9
related to several, well-known pre-, intra-, and postoperative clinical Approximately 10–20% of RD is associated with direct ocular trauma.
situations. Currently, surgery such as pneumatic retinopexy, scleral Traumatic detachments are more common in younger people. Although
buckling, and pars plana vitrectomy (PPV) is the mainstream therapeu- no studies have estimated the incidence of RD in contact sports, certain
tic modality for RD and PVR. The goal of surgery is to create chorioreti- sports (e.g., boxing and bungee jumping) are associated with an
nal adhesion around all the retinal breaks and to relive all the tractional increased risk of RD. There are also a few reports that Nd : YAG laser
force. Single-operation reattachment rates were 73% for pneumatic reti- capsulotomy10,11 is associated with an increased risk of RD.
nopexy and 82% for scleral buckling after 6 months, and multiple- As for racial difference in the incidence of RD in pediatrics, while
operation reattachment rates at 2 years were 99% for pneumatic structural abnormalities (56%), previous surgery (51%), trauma (36%),
retinopexy and 98% for scleral buckling for RD. Surgical success rates and uveitis (15%) were the main risk factors for RD in USA,12 high
for PVR have improved as techniques and instruments of vitrectomy myopia (38%), trauma (31%), structural abnormalities (17%), and
evolved. The introduction of ancillary techniques such as longer-acting previous surgery (5%) were the main risk factors in Asia.13
gases and long-term vitreous substitutes like silicone oil elevated the
success rate from 35–40% to approximately 60–75% at 6 months. Despite
these advances, more than one-fourth of initially successful cases results
in redetachment due to recurrent retinal traction. Furthermore, visual INCIDENCE OF PROLIFERATIVE
results are less satisfactory and only 40–80% of cases with anatomic VITREORETINOPATHY
success achieve ambulatory vision. As a result, PVR remains a difﬁcult
problem to manage and continuing efforts have been made to develop Published series through the 1990s to early 2000 suggest that the
other forms of therapy to inhibit the pathologic response causing trac- frequency of PVR remains largely unchanged in primary RD, with
tion. Recent efforts have been directed toward the chemical inhibition the incidence ranging from 5.1 to 11.7%.
of cellular proliferation and membrane contraction in PVR.
PATHOGENESIS OF PROLIFERATIVE
INCIDENCE OF RETINAL DETACHMENT VITREORETINOPATHY
In normal eyes, RD occurs at a rate of approximately 5 per 100 000 PVR is the result of growth and contraction of cellular membranes
people per year in the USA, and the age-adjusted incidence of within the hyaloids, retina, and retinal surface.14 These membranes
idiopathic RD is approximately 12.5 cases per 100 000 per year, or about exert traction and may cause tractional RD that opens otherwise suc-
28 000 cases per year.2,3 cessfully treated retinal breaks, creating new retinal breaks, or promot-
ing proliferation at the posterior vitreous base and anterior cortical
vitreous. This in turn causes anteroperipheral traction on the retina with
displacement of the peripheral retina toward the pars plana. Membrane
ETIOLOGY AND RISK FACTORS FOR contraction on the inner retina causes distortion and folding, resulting
RETINAL DETACHMENT in starfolds at the inferior quadrant (Figure 21.2).
Rhegmatogenous RD develops with: (1) the existence of liqueﬁed vitre-
ous gel; (2) tractional force resulting in retinal breaks; and (3) the pres-
ence of a retinal break (Figure 21.1). The most common worldwide RISK FACTORS FOR PROLIFERATIVE
etiological factors associated with RD are myopia, cataract removal, and VITREORETINOPATHY
trauma. Approximately 40–50% of all patients with RD have myopia.
RD related to myopia tends to occur in patients aged 25–45 years, while Although PVR is the most common cause of failed repair of rhegmatog-
nonmyopia RD tends to occur in older individuals. Patients with high enous RD, risk factors for PVR are related to several, well-known pre-,
myopia (>6 D), which is more common in males than females, have a intra-, and postoperative clinical situations. A number of factors
5% lifetime risk of RD. can increase the risk of PVR, including the preoperative extent of
CHAPTER 21 • Retinal Detachment and Proliferative Vitreoretinopathy
Anterior flap Operculum
and retinal tear
traction Retinal hole
Dispersed retinal Retina
Figure 21.1 Retinal tears due to vitreoretinal traction. Persistent traction frequently causes retinal detachment (A). If the traction results in a
break that is not associated with persistent vitreoretinal traction (B), the tear will act as a retinal hole and detachment is unlikely.
There are three major wound-healing phases that occur after tissue
injury: inﬂammation, proliferation, and scar modulation.20 After a
retinal break occurs, inﬂammation proceeds with the breakdown of the
blood–retinal barrier. This enables platelets to migrate to the lesion site
and release growth factors. Concurrently, extracellular matrix is pro-
duced using ﬁbrin and ﬁbronectin.21 These processes act as chemotactic
factors for attracting monocytes. Cells involved in the inﬂammatory
process during wound healing in RD include retinal pigment epithelial
(RPE) cells, macrophage-like cells, glial cells, and ﬁbroblast-like cells,
and this process triggers the onset of PVR.22 Of these cell types, RPE
cells, which are present in almost all epiretinal membranes, are the key
factor in triggering PVR development.21 RPE cells have a wide range of
activities, and can act like ﬁbroblasts and participate in ﬁbrosis,23 release
factors similar to those of glial cells, promote extracellular matrix con-
traction24 and synthesize collagen types 1, 2, and 3.25
Soluble mediators such as growth factors and cytokines26 play a role
in producing membranes which occur in PVR, and the extracellular
matrix components (most importantly, collagen and the elastic ﬁber
family) play a critical role in cellular events, including proliferation,
migration, tissue contraction, and tissue remodeling.25,27 Among the
soluble mediators, ﬁbroblast growth factor induces the proliferation of
ﬁbroblasts, which synthesize the extracellular matrix, leading to the
formation of intravitreal and periretinal membranes. In the ﬁnal process,
membrane contraction occurs, leading to tractional RD.
Figure 21.2 Starfold from proliferative vitreoretinopathy. Contraction SIGNS, SYMPTOMS, AND DIAGNOSIS
of a focal retinal surface membrane (arrow) has resulted in the
formation of a starfold. Rhegmatogenous RD presents as an accumulation of subretinal ﬂuid
with one or more retinal breaks. Symptoms such as photopsia and/or
detachment exceeding two quadrants, giant, large, multiple, or unde- increased vitreous ﬂoaters with acute posterior vitreous detachment
tected retinal breaks,15 aphakia status, vitreous hemorrhage,16 preopera- may indicate the development of a retinal break. In symptomatic eyes,
tive choroidal detachment, previous failed attempts at reattachment, retinal tears associated with persistent vitreoretinal traction indicate a
the presence of signs of uveitis, and the preoperative presence of PVR high risk for RD which may present with decreased visual acuity and/
grades A and B.17 In giant retinal tears, the PVR incidence varies from or restriction of the visual ﬁeld. The most common presentation of PVR
16 to 41%, while in penetrating ocular traumas the incidence is 10–45% is epiretinal membrane proliferation causing traction, with retinal folds
with a mean of 25%.1 In eyes with rhegmatogenous RD with grade B on the retina in an eye with rhegmatogenous RD. Other presentations
PVR, the incidence of severe PVR after surgery was reported to be include multiple retinal breaks, a vitreoretinal traction ring, and con-
25.8% when using cryotherapy and 2.2% when using argon laser pho- traction of the vitreous base.
tocoagulation.18 Intraocular hemorrhage during or after surgery, use of It is difﬁcult to diagnose PVR when there is media opacity due to
air or sulfur hexaﬂuoride (SF6), excessive cryotherapy, diathermy or corneal, lenticular, or vitreous opacities. In such cases, ultrasonographic
photocoagulation,19 repeated surgical procedures, loss of vitreous characteristics showing funnel-shaped RD with the opposition of the
during drainage of subretinal ﬂuid, and the use of vitrectomy are also posterior retina or the presence of an anterior membrane bridging the
intraoperative risk factors that increase the incidence of PVR. mouth of the funnel28 can provide evidence for a diagnosis (Figure 21.3).
SECTION 3 • Retinal Diseases Amenable to Pharmacotherapy
Figure 21.3 Ultrasonograph of an eye with rhegmatogenous reitinal
detachment with proliferative vitreoretinopathy. Figure 21.4 Correct position of scleral buckle for ﬂap retinal tear.
Table 21.1 Classiﬁcation of proliferative vitreoretinopathy (PVR) used in the silicone study
Type no. Type of contraction Location of PVR Summary of clinical signs
1 Focal Posterior Starfold
2 Diffuse Posterior Conﬂuent irregular retinal folds in posterior retina; remainder of
retina drawn posteriorly; optic disc may not be visible
3 Subretinal Posterior “Napkin ring” around disc or “clothesline” elevation of retina
4 Circumferential Anterior Irregular retinal folds in the anterior retina; series of radial folds
more posteriorly; peripheral retina within vitreous base
5 Perpendicular Anterior Smooth circumferential fold of retina at insertion of posterior
6 Anterior Anterior Circumferential fold of retina at insertion of posterior hyaloid
pulled forward; trough of peripheral retina anteriorly; ciliary
processes stretched with possible hypotony; iris retracted
Reprinted with permission from Lean J, Irvine A, Stern W, et al. Classiﬁcation of proliferative vitreoretinopathy used in the silicone study. The Silicone study
group. Ophthalmology 1989;96:765–771.
After diagnosis, PVR should be classiﬁed according to the commonly be caused by ﬁbrosis and/or altering the action of the rectus muscles.
used system presented in Table 21.1. This system distinguishes between Other complications include infection, extrusion, or intrusion of the
anterior and posterior forms of PVR, and identiﬁes proliferation as buckling element, anterior-segment ischemia, and choroidal detach-
diffuse, focal, or subretinal. While this system provides information on ment. Pneumatic retinopexy is a possible alternative to scleral buckling,
the anatomical construction of PVR, it does not indicate the biological and may be used to treat rhegmatogenous RD with retinal breaks in the
activity or prognostic factors.1 superior two-thirds of the retina. This procedure involves injecting a gas
bubble into the vitreous cavity and positioning the patient’s head such
that the retinal breaks can be closed by the bubble, while laser photoco-
agulation or cryotherapy is used for retinopexy. However, the possibility
TREATMENT OPTIONS of overlooking an existing retinal break, or creating a new break, could
be higher for pneumatic retinopexy compared to scleral buckling.
Currently available surgical options for RD management are pneumatic PPV was previously considered a second-line treatment for primary
retinopexy, scleral buckling, and PPV. There remains no consensus RD. However, a growing number of surgeons choose primary vitrec-
regarding the optimal surgical management option, and the choice is tomy for rhegmatogenous RD, in part due to the rapid advances in
generally based on many factors, including the characteristics of the instrumentation. The major advantage of primary vitrectomy is that it
retinal breaks, lens status, various patient factors (e.g., expected compli- allows a direct approach to the release of vitreous traction. Vitrectomy
ance with postoperative positioning), and surgeon preference.29 can also remove media opacities, and therefore improve intraoperative
The principles of surgical management consist of sealing all retinal visualization and control internal drainage of subretinal ﬂuid. The
breaks by making permanent scars, and relief of vitreoretinal traction. greatest problem with primary vitrectomy is the possibility of causing
Scleral buckling, including an encircling element and subretinal ﬂuid new retinal breaks and cataract formation. Furthermore, vitrectomy
drainage in some cases, relieves the vitreous traction on the retina and may be a more expensive procedure because it requires more special-
displaces some subretinal ﬂuid from the breaks, resulting in an approxi- ized operating room equipment and instrumentation.30
mation of a neurosensory retina and RPE (Figure 21.4). Complications Early surgical failures are mostly the result of failure to seal all retinal
of scleral buckling surgery include refractive change, which is typically breaks, and/or failure to relieve vitreous traction adequately. In con-
axial myopia induced by encircling elements, and strabismus, which may trast, late surgical failures are usually due to PVR, which accounts for
applied to the edges of the retinotomy site with the addition of long-
term tamponades. Most severe cases involving advanced anterior PVR
have used a posterior 360° retinotomy combined with an extensive
peripheral retinectomy and silicone oil tamponade.34 However, the
results have not been encouraging due to reproliferation causing recur-
rent macular detachment. Surgical means to reduce the risk of PVR
include removal of vitreous collagen, which is the stratum to cell attach-
ment, using wide-angle viewing systems and heavy liquids, and appli-
cation of dyes which aim at a more thorough and less traumatic removal
of vitreous and periretinal membranes.35 In addition, recent efforts have
CHAPTER 21 • Retinal Detachment and Proliferative Vitreoretinopathy
been directed toward the pharmacological inhibition of cellular prolif-
eration and membrane contraction in PVR.
PROGNOSIS WITH THE VARIOUS
It appears that the surgical success rates for pneumatic retinopexy are
either similar to or slightly lower than those for scleral buckling, and the
risk of late redetachment is similar for pneumatic retinopexy and scleral
buckling.30 In a 2-year follow-up study, single-operation reattachment
rates were 73% for pneumatic retinopexy and 82% for scleral buckling
after 6 months, and multiple-operation reattachment rates at 2 years
were 99% for pneumatic retinopexy and 98% for scleral buckling.36
More recently, a few prospective randomized trials revealed that
there was no statistically signiﬁcant difference in single-operation
success rates or visual outcomes when comparing primary vitrectomy
with scleral buckling for the treatment of rhegmatogenous RD.37,38
However, faster foveal reattachment may be an advantage of PPV. In
a nonrandomized series of 33 cases of macular-off RD, serial optical
coherence tomography examinations showed no primary vitrectomy
patients had subfoveal ﬂuid while approximately one-third of scleral
buckling patients had subfoveal ﬂuid after the operation.39
Surgical success rates for PVR have improved as vitrectomy tech-
niques and instruments have evolved. The introduction of ancillary
techniques such as longer-acting gases and long-term vitreous substi-
tutes like silicone oil have elevated the success rate from 35–40% to
B approximately 60–75% at 6 months.40,41 Despite these advances, more
than 25% of initially successful cases result in redetachment due to
Figure 21.5 Ability of perﬂuorocarbon liquids to reattach recurrent retinal traction. Furthermore, visual results are less satisfac-
mechanically posterior retina in proliferative vitreoretinopathy. tory and only 40–80% of cases with anatomic success achieve ambula-
Epiretinal membranes cause folding and shortening of the retina in tory (5/200 or better) vision.42 As a result, PVR remains a major problem,
both anteroposterior and circumferential directions (A). After and continuing efforts have been made to develop other forms of
performing membranectomy on posterior region of the retina, therapy to inhibit the pathological response causing traction. Recent
perﬂuorocarbon liquid may be used to reattach the posterior retina efforts have been directed towards chemical inhibition of cellular pro-
and aid in removal of peripheral epiretinal membrane (B). liferation and membrane contraction for PVR.
the majority of failures following RD surgery. Surgical procedures used
to repair RDs associated with PVR include scleral buckling, vitrectomy, ADJUNCTIVE THERAPIES
membrane peeling, relaxing retinotomies, the use of liquid perﬂuoro-
carbons, and internal tamponade with gas or silicone oil (Figure 21.5).31 Although PVR is currently primarily managed surgically, ongoing
In the early stages of PVR, buckling and encircling procedures may efforts seek to identify adjuvant therapies that might inhibit PVR devel-
close all retinal breaks with release of circumferential traction caused opment. No matter how thoroughly vitrectomy is performed, it is virtu-
by the vitreous base.17 A moderately wide, broad silicone band (5–7 mm) ally impossible to prevent some level of cell adhesion and pathological
extending from the ora serrata to the equator is required to reduce the change. Control of the biological processes involved in proliferation
vitreous traction.13 In addition, retinopexy with cryotherapy, diathermy, and wound-healing would improve the success rate of surgery for
and photocoagulation can be used to treat deﬁnite retinal breaks, thus primary RD and PVR.
minimizing further RPE cell dispersion, postoperative inﬂammation, Daunorubicin was the ﬁrst adjunct agent to be studied in a random-
and breakdown of the blood–retinal barrier. While there is no standard- ized controlled trial for the management of PVR, and was found to
ized approach to PVR treatment, types 1 and 2 affecting fewer than two reduce the number of reoperations within 1 year.43 Recent advances in
quadrants (classiﬁcation system by the Silicone Oil study) can be suc- the sustained release of daunomycin achieved by a single intravitreal
cessfully treated using buckling procedures. application of liposome encapsulation44 may be very useful for future
PPV is indicated in cases with no deﬁnite retinal breaks with trac- treatment strategies.
tional membranes causing RD, or in cases where the retinal breaks A randomized controlled trial in the UK reported that adjuvant
cannot be sealed by scleral buckling alone.14 However, in complex PVR 5-ﬂuorouracil and heparin prevented PVR. In that study, the combina-
cases, it is necessary to perform a vitrectomy with membrane peeling tion treatment resulted in a signiﬁcant reduction in the rate of postopera-
and a gas or silicone oil tamponade.32 Moreover, a relaxing retinotomy tive PVR development.45 However, subsequent studies failed to show
and retinectomy may be required to attach the retina to the RPE in such any beneﬁt of this combination treatment, and indeed one of the study
complex cases.33 Once all traction is relieved, photocoagulation is results showed worse outcomes in macula-sparing RDs patients.46,47
Many drugs, such as colchicine, corticosteroids, retinoids, and 18. Bonnet M, Guenoun S. Surgical risk factors for severe postoperative
heparin, might be useful for inhibiting PVR development at speciﬁc proliferative vitreoretinopathy (PVR) in retinal detachment with grade B
PVR. Graefes Arch Clin Exp Ophthalmol 1995;233:789–791.
stages. More detailed understanding of the pathophysiology underly- ,
19. Jaccoma EH, Conway BP Campochiaro PA. Cryotherapy causes extensive
ing PVR may lead to the development of effective prophylactic and/or breakdown of the blood–retinal barrier. A comparison with argon laser
adjunct therapies. Further work is necessary to identify optimal adjunct photocoagulation. Arch Ophthalmol 1985;103:1728–1730.
therapies for the management of RD and PVR. ,
20. Wiedemann P Weller M. The pathophysiology of proliferative
vitreoretinopathy. Acta Ophthalmol Suppl 1988;189:3–15.
21. Casaroli Marano RP Vilaro S. The role of ﬁbronectin, laminin, vitronectin
and their receptors on cellular adhesion in proliferative vitreoretinopathy.
Invest Ophthalmol Vis Sci 1994;35:2791–2803.
SUMMARY AND KEY POINTS ,
22. Baudouin C, Hofman P Brignole F, et al. Immunocytology of cellular
SECTION 3 • Retinal Diseases Amenable to Pharmacotherapy
components in vitreous and subretinal ﬂuid from patients with proliferative
vitreoretinopathy. Ophthalmologica 1991;203:38–46.
Current methods of surgical management of RD and PVR are pneu- 23. Lee SC, Kwon OW, Seong GJ, et al. Epitheliomesenchymal
matic retinopexy, scleral buckling, and PPV. The principles of surgical transdifferentiation of cultured RPE cells. Ophthalmic Res 2001;33:80–86.
management consist of sealing all retinal breaks and relief of vitreoreti- 24. Glaser BM, Cardin A, Biscoe B. Proliferative vitreoretinopathy. The
mechanism of development of vitreoretinal traction. Ophthalmology
nal traction. However, although surgical success rates for PVR have 1987;94:327–332.
improved as vitrectomy techniques and instruments have evolved, ,
25. Hiscott P Sheridan C, Magee RM, et al. Matrix and the retinal pigment
more than 25% of initially successful cases result in retinal redetach- epithelium in proliferative retinal disease. Prog Retin Eye Res
ment due to recurrent tractional proliferation. This of course, results in 1999;18:167–190.
26. Wiedemann P. Growth factors in retinal diseases: proliferative
suboptimal visual results as well. vitreoretinopathy, proliferative diabetic retinopathy, and retinal
Recent efforts have therefore been directed toward pharmacologic degeneration. Surv Ophthalmol 1992;36:373–384.
inhibition of cellular proliferation and membrane contraction with 27. Jerdan JA, Pepose JS, Michels RG, et al. Proliferative vitreoretinopathy
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processes leading to retina damage after detachment, and knowledge 29. Schwartz SG, Flynn HW. Primary retinal detachment: scleral buckle or pars
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