Introduction

Retinal detachments (RD) occurring in the context of ocular inflammation are a particular challenge both to the vitreoretinal surgeon and to the uveitis specialist. Most often they occur during or following an episode of intraocular infection and are most commonly seen in eyes having suffered from a viral retinitis. When they are not related to ocular infection, their diagnostic and therapeutic approach may be difficult, since different forms of retinal involvement suppose different treatments and prognosis. Serous retinal detachment (SRD) is the form most commonly associated with active, purely inflammatory conditions and, often, its presence helps to establish the diagnosis, as in the case of Vogt–Koyanagi–Harada disease (see Chapter 75, Vogt–Koyanagi–Harada disease). Not infrequently, it is misdiagnosed for a rhegmatogenous retinal detachment (RRD). However, the management of SRD is entirely pharmacologic, aimed at controlling the intraocular inflammation, and not surgical. The visual prognosis in most cases of SRD is excellent provided that the immunosuppressive agents have been introduced at a sufficient dose to lead to rapid resolution, and tapering is done slowly. RRD in the setting of active uveitis is thankfully rare, but its presence, even with modern vitreoretinal surgical techniques, results in a guarded visual outcome. Tractional retinal detachment (TRD) is possible in both infectious and noninfectious uveitis whenever vitreous inflammation/organization develops in an eye without posterior vitreous detachment (PVD) or when proliferative vitreoretinopathy (PVR) complicates the course of intraocular inflammation. Combined forms of RD are also possible; it is crucial to establish the exact mechanism of visual deterioration in every single case, allowing a better therapeutic approach.

Epidemiology

A systematic review of population-based studies on RRD published between 1970 and 2009 found a reported incidence between 6.3 and 17.9 for 100 000 people/year, with significant geographical variations.¹ It is widely accepted that RRD occurrence varies with ethnicity and is strongly associated with increasing age, myopia, vitreoretinal degeneration and following cataract surgery.^2,3 Uveitis itself has not been considered among the predisposing conditions to develop RRD. However, a retrospective study conducted in the Netherlands found a prevalence of RRD of 3.1% among 1387 uveitic patients, suggesting inflammation as an independent risk factor for its development.⁴

Not all types of uveitis carry the same risk of RRD; this complication is most commonly seen in posterior uveitis from infectious etiology, with the highest risk in viral retinitis cases. Acute retinal necrosis (ARN) (see Chapter 88, Acute retinal necrosis syndrome) evolves to RRD in more than 50% of cases, in a median time of 53 days after presentation.⁵ This risk is even higher for progressive outer retinal necrosis (PORN), in which almost 70% of affected eyes will develop RRD soon after presentation.⁶ For cytomegalovirus (CMV) retinitis (see Chapter 81, HIV-associated infections), even though the course of the disease has positively changed with the introduction of the HAART therapy, the rate of RRD remains as high as 2.3/100 eye-years.⁷

Parasitic infections can lead to RD when a choroidal process extends to the retina and vitreous or when a retinal process causes overlying vitreous to condense and contract. Toxoplasmic retinochoroiditis (see Chapter 85, Ocular toxoplasmosis) presents a risk of RRD of 3.5–6%.^8–10 In the subset of patients addressed for vitreoretinal surgery, Adan et al. found 53.3% of cases of RD, most of them with pure RRD, but also some cases of combined tractional and RRD.¹¹ Exudative detachments are rarely associated with ocular toxoplasmosis but have been cited in the literature.^12,13 Vision-threatening features in ocular toxocariasis (OT) (see Chapter 86, Helminthic disease) are mainly severe vitritis, cystoid macular edema and tractional detachment of the macula. A retrospective series on OT found a prevalence of macular traction of about 30%, regardless of the site where the choroidal granuloma was located. In peripheral lesions with retinal traction, TRD occurs in about 40% of cases.^4,14

Among noninfectious uveitis, the risk of RRD is less than 1%. Most patients developing retinal tears and detachments appear to do so as a result of concomitant retinal pathology, often in areas unrelated to sites of inflammation. However, inflammatory processes affecting the vitreous base may present an exception to this rule. Pars planitis, when untreated for a prolonged period of time or if severe, is known to develop TRD¹⁵ and retinoschisis.¹⁶ The differentiation between true retinoschisis and TRD may sometimes be very difficult, especially for those lesions situated in the far periphery.¹⁷ Sarcoidosis is also known to develop various forms of RD (see Chapter 78, Sarcoidosis), though this complication is rare in this condition. Serous RD,¹⁸ RRD,¹⁹ retinal pigment epithelium (RPE) detachments,²⁰ and even a rare case of necrotizing retinitis with subsequent RRD,²¹ were described in the context of ocular sarcoidosis, but mostly as isolated cases. Retinal tears and RRD are rarely found in relation to Behçet’s disease, even though detailed fundoscopy should be done periodically in these patients, mainly when vitreous inflammation is important. A case of RRD secondary to a macular hole in a young patient with Behçet uveitis²² has been reported, stressing the role of recurrent vitritis in the pathogenesis of this complication (see Chapter 77, Autoimmune retinopathies).

Pathophysiology

The nature of the inflammatory or infectious process determines the mechanism by which the detachment occurs, and provides an indication as to the means by which it can be resolved. Serous RD is usually the result of an immune-mediated assault to the choroid or the RPE. Its follows from loss of the tight junctions between retinal endothelial cells, leading to increased outward flow of fluid from retinal vasculature, and a failure of the compensatory pump function of RPE cells. Disruption of the normal oncotic gradient between the vitreous cavity and the choroid may also compromise passive transfer mechanisms responsible for a good portion of normal fluid flow to the choroid. Inflammatory mediators modulate vascular permeability and may have a role on the modulation of chloride receptors such as CLIC4 necessary for retinal attachment.^23,24 Resolution of a serous detachment requires one to re-establish the status quo by inhibiting both humoral and cellular inflammatory mechanisms through appropriate systemic or local immunosuppression (Fig. 112.1).

Fig. 112.1 Serous retinal detachment in a patient with Vogt–Koyanagi–Harada disease. Detachments are usually bullous, with shifting fluid but without undulating retinal surface. Hyperemia of the optic nerve head is often present.

In the case of both RRD and TRD, vitreous body traction plays a predominant role. In RRD associated with toxoplasmosis, active toxoplasmic retinochoroiditis often precedes or is concurrent with the development of the RRD.⁸ Inflammation not only enhances vitreous liquefaction but also leads to cross-linking between collagen fibrils, particularly those close to the retinal interface, leading to the formation of an anomalous PVD and retinal tears.^25,26 Vitreal strands between the optic disk and the ocular toxocariasis granuloma are present in nearly 50% of patients (Fig. 112.2). These strands are often the source of retinal traction and detachment. Contraction of the vitreous base, particularly seen in chronic longstanding uveitis, leads to the development of fibrous or fibrovascular bands, which can be very adherent to the underlying retina.^26,27 Their removal can be quite challenging at the time of surgery (Fig. 112.3).

Fig. 112.2 Fundus photograph from an ocular toxocariasis case. A peripheral granuloma causes a tractional retinal detachment in the central retina.

Fig. 112.3 (A) Histopathological section in a patient with pars planitis. Fibrous proliferation (*) leads to vitreous contraction between the pars plana (PP) and the retina (R). This tissue may be particularly difficult to remove surgically. (H&E ×110; courtesy of Dr Chi-Chao Chan, National Eye Institute, Bethesda, United States.) (B) Artist rendition of the pars plana exudation leading to vitreous base fibrosis and traction on the peripheral retina.

High levels of s-ICAM1 (type 1 soluble intercellular adhesion molecule) are found in vitreous from uveitic eyes complicated by RD similar to what has been observed in cases of proliferative vitreoretinopathy (PVR) where it is felt to perpetuate a cytokine-mediated vascular reaction which may contribute to PVR formation.^28–30 It correlates positively with vitreous levels of TNF-α (tumor necrosis factor-alpha), a cytokine with a key role in the initiation of the inflammatory cascade and the pathogenesis of uveitis.³¹

Herpetic retinal infections (CMV, HSV, VZV) are characterized by retinal necrosis leaving in its wake a diaphanous glial membrane (Fig. 112.4). Depending on the interplay between the virus and the host immune system, it is associated with moderate to severe vitreous inflammation. Cytomegalovirus retinitis is quintessentially seen in the context of AIDS or severe immunosuppression. It still today remains an AIDS-defining infection but is also seen in patients who fail to respond, become intolerant of, or stop responding to highly active antiretroviral therapy (HAART). Traditionally, it was not associated with vitreous inflammation and therefore, detachments were rarely complicated by proliferative vitreoretinopathy. In the HAART era, the frequency of an inflammatory response, late detachments and PVR has increased with some series reporting up to 30% of CMV retinitis cases complicated by PVR.³² The incidence of RD is highest among newly diagnosed patients (within 45 days of diagnosing a CMV retinitis) at 4.9/100 eye years, while the overall rate among AIDS patients with CMV retinitis is 2.3/100 eye years.⁷ Additional risk factors for RD include large lesion size, anterior lesion location, associated retinal pathology (e.g., myopia) and older age.^33,34 Local and systemic therapy might reduce slightly the risk of RD possibly due to a more rapid resolution of retinitis.³⁵ Most detachments occur once the initial infection has subsided. The healed retinitis leaves a thin glial sheet above which an epiretinal membrane, possibly containing condensed vitreous, can be found (Fig. 112.5).³⁶ Vitreoretinal gliosis is often present at the interface between normal and abnormal retina on optical coherence tomography (OCT) examination but is difficult to visualize clinically. It is possible that the gliosis contributes to the formation of retinal detachments in these patients.

Fig. 112.4 (A) Histopathological section of the retina in acute retinal necrosis showing a sharp border between healed and affected tissue. (B) Histopathological section of the retina in cytomegalovirus retinitis, showing also a sharp border in the healed phase.

Fig. 112.5 Artist rendition of a retinal detachment following cytomegalovirus retinitis. Atrophic scars of healed retinitis often harbor retinal breaks.

Acute retinal necrosis (ARN) is characterized by large, peripheral, often confluent zones of retinitis.^37–39 It is pathologically characterized by full-thickness retinal necrosis and occlusive vasculitis (Fig. 112.4B).⁴⁰ Vitreous involvement, often not present initially, develops within a few days and can obliterate the view of the posterior pole. A more aggressive form starting at the posterior pole called progressive outer retinal necrosis (PORN) affects also all retinal layers and represents an ophthalmic emergency since it may lead to complete blindness within hours if not treated aggressively.^41–43 In both cases, detachments occur due to vitreous traction on the atrophic retina, sometimes following the occurrence of a PVD and when severe inflammation is present, they may occur even before resolution of the active retinitis. Retinal detachments in ARN are frequently complicated by PVR, which is often extensive at the vitreous base. Retinal breaks are usually multiple and located at the juncture between normal and gliotic retina. Vitreoretinal adhesions are common and the retinal detachment has both tractional and rhegmatogenous components (Fig. 112.6).

Fig. 112.6 Artist rendition of a retinal detachment associated with acute retinal necrosis showing vitreous strands, vitreous base fibrosis and retinal thinning, tears and preretinal fibrosis. Large tears form in areas of retinal gliosis. The more extensive the area of gliosis, the more probable is the development of a detachment.

Clinical examination and findings

As stated above, RDs in uveitis can arise in a number of ways. Not infrequently, TRD, even schisis cavities, can be misdiagnosed as RRD (Fig. 112.7).¹⁶ As part of the initial work-up, it is important to establish the nature of the detachment, the etiology and severity of ocular inflammation or infection, and the status of the retina and vitreous. In particular, it is important to determine the relationship between the detached retina and the area of retinal inflammation or infection, the presence or absence of a PVD, and the presence of peripheral vitreous base fibrosis and foreshortening. These observations and work-up are often hampered by poor visualization resulting from posterior synechiae, cataract, vitreous haze or cellular infiltration. In infectious cases, particularly ARN, vitreous inflammation may increase shortly after initiating treatment to the point where it is impossible to visualize the fundus. Analogous to trauma cases, it is important in these cases to document, as early as possible, findings in the vitreous and retina.

Fig. 112.7 Peripheral traction due to vitreous bands and contraction in a patient with pars planitis and neovascularization of the vitreous base causing exudation into the subretinal space. One of the vitreous bands is visible on the retina surface.

When visualization becomes inadequate, ancillary tests may be required. To evaluate the macular area through a small pupil, a nonmydriatic camera, SLO (scanning laser ophthalmoscopy), or OCT may be useful. Unfortunately, they do not give any information on the condition of the peripheral retina. B-scan ultrasonography (both 10 and 50 MHz) is probably the most useful tool for the evaluation of the peripheral fundus. Uveitis-related RD often has a highly reflective posterior hyaloid when detached (which can even mimic an RD).⁴⁴ Occasionally, during active inflammation, fine echoes within the retrohyaloid space are visible, corresponding to inflammatory cells within the vitreous. If visualization of the vitreoretinal interface becomes difficult and therapy with intravitreal steroids is envisaged, triamcinolone will improve the ultrasound signal and facilitate visualization of posterior structures.⁴⁵ The presence of a thickened choroid (≥2 mm thickness) and the asymmetry between the two eyes can help confirming the diagnosis of a choroidal inflammation in the involved eye.⁴⁴ Choroidal detachments are not infrequent, and their anterior extent needs to be defined.

Ciliary body detachments may develop as a result of uveitis, causing or predisposing to hypotony. The UBM (ultrabiomicroscopy) is the preferred tool to visualize the ciliary body. Using a UBM, it is also possible to assess the peripheral vitreous, in particular if it has become adherent to the posterior iris surface causing posterior displacement of the iris plane (an indirect sign of vitreous base fibrosis and likely foreshortening of the retina) (Fig. 112.8).^46,47

Fig. 112.8 Ultrasound biomicroscopy of the pars plana region of a patient with sarcoidosis. Vitreous condensation and contraction onto the posterior iris surface has also led to traction and detachment on the ciliary processes.

Tears in inflammatory retinal detachment are usually localized in areas suggested by classic teaching except in chronic peripheral uveitis (such as pars planitis) where there is an important component of anterior traction due to vitreous base foreshortening. Combined tractional–rhegmatogenous detachments are also common but are usually clearly evident from the retinal contour. In post-herpetic detachments, tears are often located at the margin of the atrophic scar or at the insertion of the posterior hyaloid on the retinal surface.

Management

As with any retinal detachment repair, the decision to intervene is based on an analysis of the potential risks contrasted with the probability of anatomic success and vision improvement. In the absence of active inflammation, most cases respond as if they were uncomplicated retinal detachments and thus, the benefit outweighs the surgical risk. With active inflammation, or in AIDS patients, the postoperative results may be much more limited. Here, timing and modifications of existing surgical techniques may be required.

RD with active inflammation

Results of surgery performed on retinal detachments during active inflammation have generally been poor.^4,48,49 Inflammation leads to poor postoperative visualization and development of fresh membranes on the retinal surface and in the retrolenticular space. It is crucial to adequately and aggressively manage the inflammatory component with a combination of systemic and local therapy. Systemic therapy should be initiated prior to surgery. The choice will depend on the nature of the inflammation and previous response to treatment. If the iris can be manipulated during surgery, prostaglandin inhibitors should be added topically as well as systemically starting the day prior to surgery. This can significantly reduce anterior segment inflammation and is commonly done in cataract surgery on uveitis patients.⁵⁰ At the end of surgery, periocular and intraocular steroids should be considered. The use of a long-acting steroid preparation might reduce the severity of any recurrence developing several days or weeks after surgery.

In general, better surgical success is obtained when a more aggressive approach is taken. The lens, if present, is removed and an IOL is placed in the bag. Following a standard pars plana vitrectomy, which preferably is performed with small-gauge surgery, a posterior vitreous detachment is induced and carried out to the vitreous base (Fig. 112.9A). This can be facilitated by the use of intravitreal triamcinolone or a coloring agent. If it is not possible to remove the posterior hyaloid completely, the vitreous is shaven down to the retinal surface (Fig. 112.9B). This is particularly important at the vitreous base (Fig. 112.9C), as there will be a tendency for any remaining scaffold to contract and pull on the ciliary body and peripheral retina potentially leading to hypotony and/or recurrent detachments (Fig. 112.8). Membranes present on the retinal surface are peeled; given their tenacity, this is often best done using a bimanual technique with a pic and a forceps (Fig. 112.9D).

Fig. 112.9 Vitrectomy for retinal detachment in patients with active uveitis. (A) A standard pars plana vitrectomy is carried out, followed by the induction of a posterior vitreous detachment. The vitrectomy is usually initiated after removal of the crystalline lens and its replacement with an intraocular lens. (B) When the posterior hyaloid cannot be easily detached even with the use of a coloring agent, the vitreous is resected up to the surface of the retina. (C) Resection of the vitreous is carried out over the vitreous base, where the vitreous remnants are shaven down to the retina surface. (D) Dissection of membranes present on the retinal surface is best achieved using a bimanual technique, the use of perfluorocarbon and a chandelier lighting system.

Illumination is provided by a chandelier or transscleral illumination system. Peeling is also facilitated by using perfluorocarbon, which acts as a “third” arm, providing posterior stabilization to the membranes being peeled. Once the retina is fully reattached under perfluorocarbon, to avoid aggravating existing inflammation, the edges of the tears are treated by photocoagulation. Cryotherapy should be avoided, as it enhances breakdown of the blood–ocular barrier and can increase postoperative inflammation.⁵¹ Silicone oil is the preferred tamponading agent, as it will allow continued visualization of the retinal structures while the inflammation is brought under control (Fig. 112.10). It also limits the accumulation of proinflammatory cytokines in the vitreous cavity.⁵² The oil can be removed when the inflammation is brought fully under control.

Fig. 112.10 Once the retina is mobilized, an air–fluid exchange is performed to reattach the retina. Retinotomies are done if traction is not fully relieved. Alternatively, silicone oil–perfluorocarbon exchange can be undergone.

RD with retinal necrosis

Cytomegalovirus retinitis

In selected cases of CMV-associated retinal detachments, photocoagulation may be effective in delimiting or demarcating the retinal detachment.^54–56 It can lead to a significant delay in macular detachment. Delay in intraocular surgery in these patients is a valid strategy, as following successful reattachment, several studies have suggested a variable loss of vision possibly related to microangiopathy, optic neuropathy or silicone-oil-related toxicity.^57–61 Once a surgical option is chosen, retinal detachments due to CMV, whether or not associated with PVR, should be approached in a standardized fashion. The risk of recurrence or progression of CMV should be assessed in conjunction with the treating internist as it will determine the choice of tamponade and the need for concurrent cataract extraction.

The surgery begins with a standard three-port vitrectomy (Fig. 112.9). When pre-existing vitreous separation is present, the posterior hyaloid is identified and resected up to the posterior margin of the vitreous base. In some cases, however, the vitreous has not detached posteriorly. If it can be mechanically engaged and easily elevated from the retina, this is done to create a posterior vitreous separation. In some cases, this technical separation cannot be safely accomplished. An attempt should be made to resect the vitreous as close to the surface of the retina as possible, without inducing a vitreous detachment. In cases in which CMV has caused necrosis of a large area of retina, an en bloc dissection of diaphanous retina and vitreous is possible but should in most cases follow separation of the vitreous from surrounding healthy retina, or at least after it has been shaven off the retinal surface. The edges of retinal breaks or the area of resection are marked with intraocular diathermy (Fig. 112.11). This makes later identification easier. Internal drainage of subretinal fluid in conjunction with air–fluid or fluid–silicone exchange is performed to flatten the retina (Fig. 112.10). The retinal breaks are surrounded with endophotocoagulation (Fig. 112.12).

Fig. 112.11 The retinal breaks are identified and marked with diathermy, particularly if a gas exchange is chosen to flatten the retina.

Fig. 112.12 Once attached under air, perfluorocarbon, or silicone oil, the edges of all tears and retinotomies are treated with endolaser.

Many surgeons advocate demarcating the atrophic areas with laser, as well as those regions that are likely to harbor retinal breaks. In certain circumstances, scatter photocoagulation applied to the lower hemisphere up to the edge of the inferior vascular arcade, can help mitigate the appearance of a later detachment, particularly if CMV progression in this area is expected in the coming months. A silicone–air exchange or air–gas exchange is performed at this point. The choice will depend on the configuration of the detachment, and the likelihood of recurrent activity. If progression is likely, silicone oil is a better and more permanent choice. Postoperatively, the patient is kept facedown for 12 hours, after which time special positioning is not necessary. Careful follow-up is required postoperatively to observe for the complications of silicone oil, to monitor for recurrence of infection, and to detect recurrent retinal detachment.^{34,57,58,60–65}

Redetachment of the retina may occur at any time postoperatively and may be caused by new retinal breaks or reopening of previously treated breaks. Typically, the recurrent retinal detachment is shallow and located inferiorly, where the silicone bubble may not be entirely in contact with the retina. If the redetachment is localized and extramacular, observation is usually the best strategy. If the macula is threatened or detached in an eye with previously good vision, then reoperation may be warranted. Often, drainage of subretinal fluid combined with injection of more silicone and then further photocoagulation is the treatment of choice. If one is working through a pars plana approach with silicone oil in the eye, observation of the field may be compromised by early cataract or by optical aberrations caused by the oil. Occasionally, the oil must be removed and the retina reattached, as described above, before the oil is reinjected.

Lensectomy may be necessary with or without implantation of an intraocular lens, maintaining the posterior capsule. Later capsular opacification is common, however, and one should consider primary capsulotomy in selected cases.⁶⁶ An inferior iridectomy must be performed in aphakic eyes and should be considered in pseudophakic eyes to prevent pupillary block.

If intraocular lens implantation is performed primarily (to correct for anisometropia), later at reoperation, or to correct for a visually significant postoperative cataract, the appropriate intraocular lens should be chosen.^67,68 A planoconvex polymethylmethacrylate (PMMA) or hydrophobic acrylic intraocular lens provides the ideal optical correction. Engstrom et al. reported satisfactory results with simultaneous lensectomy and intraocular lens implantation at the time of vitrectomy and silicone oil injection.⁶⁷ This strategy is used to avoid silicone-oil-induced anisometropia and to obviate the need for later cataract removal, as silicone oil almost always induces cataract formation.⁶⁶

Acute retinal necrosis

The operation should be tailored to the severity of the disease. In most cases, traction from a partially detached vitreous on the vascular scaffold remaining in the friable retinal tissue after the infection subsides, leads to the presence of multiple holes, low-lying detachments and PVR, both anterior and posterior.

A standard three-port vitrectomy is performed (Fig. 112.9). As in CMV cases, it is important to keep the infusion pressure low. The optic nerve in these patients does not tolerate standard infusion pressures. Looking at the nerve to avoid a pulsatile perfusion at the onset of surgery, and periodically during surgery, can avoid further loss of vision from prolonged retina anoxia. In most cases, the crystalline lens and in some cases the intraocular lens will be removed to expose the full extent of the vitreous base so that all scarring can be removed and basal vitreous traction can be eliminated.

In almost all cases, a spontaneous posterior vitreous detachment has occurred. The vitreous gel must be resected out to the margin between healthy and atrophic retina or to the posterior margin of the vitreous base (Fig. 112.13). Posterior epiretinal membranes overlying healthy retina are identified and removed with picks and forceps. A chandelier lighting system may facilitate this maneuver (Fig. 112.14).

Fig. 112.13 In acute retinal necrosis syndrome, a posterior vitreous detachment is usually present. It is carried out to the vitreous base.

Fig. 112.14 In acute retinal necrosis syndrome, posterior epiretinal membranes are identified and removed with pic and forceps.

Once the posterior healthy retina is free of membranes, perfluorocarbon is used to tamponade this retina out to the edge of atrophic retina. If detached, it should be removed en bloc. Its diaphanous nature makes it difficult to peel off membranes, and it does not coagulate well with laser. In any case, this is not seeing retinal tissue. Larger vessels, even though these are attenuated, should be treated with diathermy as they may bleed. To facilitate removal, deep scleral depression can be used. This may lead to a 360° retinotomy leaving a fairly central area of viable healthy retina.

Once the vitreous and preretinal membranes and detached atrophic retina has been removed, remaining retinal breaks are identified and marked with endodiathermy, under perfluorocarbon the edge between healthy and any remaining atrophic retina, as well as the free edge which was created earlier are treated by endophotocoagulation, placing several rows of laser along the edge of healthy retina.

If there is a need for peripheral support, particularly inferiorly, an inferior encircling band or a complete scleral buckle can be placed. However, in many cases it is not needed, and best avoided if possible as it can lead to choroidal ischemia and compromise residual retinal function.

Silicone oil is used to tamponade the retina. The oil should be removed in 2–6 months if possible to avoid the long-term complications related to its presence.

In managing PORN-related retinal detachments, the surgical principles are identical. The extent of the necrosis, however, is almost always greater than in patients with ARN-related retinal detachments, so extra care must be taken with vitreous manipulation, and the amount of photocoagulation required is often much more extensive in an effort to surround and preserve the macular region.^41,69

Prognosis

Visual restoration after SRD is usually good, with most eyes achieving >20/40 after adequate treatment. Visual function after uveitis-associated RRD is frequently guarded, with almost 70% of eyes with <20/200 if the RD is repaired during active inflammation. This poor visual prognosis is related both to the ocular inflammation and to the high frequency of proliferative vitreoretinopathy (PVR) appearing after surgery. In order to mitigate the effects of inflammation, it is necessary to anticipate its consequences and hence use silicone oil, even though there is little evidence of PVR at the time of surgery, or remove a perfectly clear crystalline lens in order to complete the vitreous resection up and over the vitreous base. In viral retinitis, a similar approach is often required. In addition in these conditions, the surgery should be carried out as much as possible with a low intraocular pressure, as the circulation through the optic nerve may be occluded at even standard infusion pressures. Proliferative retinopathy (PVR) is enhanced by inflammatory cytokines normally present in the anterior chamber and vitreous body of eyes with uveitis. Reducing these can improve the prognosis and implies a concerted local and systemic effort to minimize intraocular inflammation. It is best achieved as a team effort between the vitreoretinal surgeon and the uveitis specialist.

Conclusion

Management of retinal detachments in patients with inflammation or infection demands not only knowledge of surgical options, but also a good grasp of the underlying disease, an estimate of the probable post-operative course as well as the likelihood of recurrence. A multidisciplinary approach is most likely to provide the optimal outcome in most settings. While in the past, visual results after surgery were relatively poor, the advent of better equipment, less traumatic surgical approaches, and a better understanding of the pathophysiological processes at hand have improved both short-term and long-term outcomes. Both timing and extent of surgery are critical issues which vary depending on the etiology. Larger series obtained by combining results from several different centers will help to define more precisely these parameters in years to come.