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Chapter 137 – Serous Detachment of the Neural Retina

Chapter 137 – Serous Detachment of the Neural Retina

 

RAJIV ANAND

 

 

 

 

 

DEFINITION

• An elevation of the neural retina due to the accumulation of subretinal fluid in the absence of a retinal break or significant preretinal traction.

 

KEY FEATURES

• Dependent subretinal fluid that shifts with change in head position.

• Lack of a rhegmatogenous or tractional component.

• Secondary to local ocular or systemic etiology.

 

ASSOCIATED FEATURES

• A breakdown in the blood–retina barrier.

• Absence of corrugated or fixed retinal folds.

• Clear or lipid-rich exudative subretinal fluid.

• Local ocular-associated disease, such as tumor, inflammation, vasculopathy.

• Systemic associated disease, such as hypertension, acute fluid retention.

 

 

 

INTRODUCTION

Serous detachment of the neural retina (serous retinal detachment) has been the subject of intense experimental scrutiny as the mechanisms that keep the neural retina attached to the underlying retinal pigment epithelium have become better understood. Normal retina is kept dehydrated and in apposition to the choroid by the blood–retina barrier and active cellular transport. Serous or exudative retinal detachment develops secondarily when the blood–retina barrier is damaged. In the absence of a retinal break, the diagnosis of serous, non-rhegmatogenous retinal detachment may be fairly straightforward; however, management often is fraught with difficulty. A wide variety of local and systemic pathology can cause secondary subretinal fluid accumulation. In this chapter the important clinical entities are discussed briefly and an attempt is made to summarize the pathogenic mechanisms in a logical fashion.

EPIDEMIOLOGY AND PATHOGENESIS

The cellular and fluid flow mechanisms that keep the neural retina attached to the retinal pigment epithelium (RPE) have been investigated fairly thoroughly. It is accepted that the vitreous gel and interdigitations between the photoreceptor outer segments and the RPE provide very little mechanical support for the retina. On the other hand, fluid flow dynamics play a major part in providing a suction force that keeps the retina attached to the RPE.[1] A significant suction force is generated by ionic flow from the RPE to the choriocapillaris. This is demonstrated in freshly enucleated animal eyes and also in human eyes, in which detaching healthy retina is difficult. The colloidal osmotic forces in the choriocapillaris provide an additional unidirectional flow of fluid from the posterior segment of the eye toward the vortex veins and then to the orbital venous system. The retina is kept dehydrated by tight junctions between the capillary endothelial cells. In addition, tight junctions also exist between the adjacent RPE cells, which provide a barrier between the sensory retina and the highly vascularized choroid.

The pump and metabolic functions of the RPE cells play the predominant role in keeping the neural retina attached as well as dehydrated. Experimental studies by Marmor and colleagues[2] [3] show that damage to the RPE barrier is necessary before large molecules such as albumin can diffuse into the subretinal space from both the vitreous and the bloodstream. Even when a breakdown in the blood–retina barrier occurs, as long as the RPE cells are capable of pumping out the extra fluid, subretinal fluid does not accumulate. If the function of the RPE is impaired and a breach in Bruch’s membrane occurs, such as in choroidal tumors or choroiditis, fluid accumulates in the subretinal space. At this stage, destructive procedures (e.g., radiotherapy, cryotherapy, or laser) work by obliterating the primary site of blood–retinal barrier breakdown and provide adhesion to the underlying choroid. Also, the surrounding healthy RPE cells resume their active outward transport and thereby reattach the retina. Figure 137-1 illustrates the major forces involved in keeping normal retina attached.

Three major pathological mechanisms are implicated in the accumulation of subretinal fluid:

• A net increase in fluid flow into the subretinal space (e.g., a vascularized tumor with incompetent vasculature)

• An impaired outflow that disrupts the normal anterior-to-posterior egress of fluid (e.g., choroidal inflammation or orbital infiltration)

• A breakdown of the blood–retina barrier with impairment of the RPE fluid pump (e.g., central serous chorioretinopathy, inflammation)

Only one mechanism need be present for serous detachment of the neural retina to occur, but all three mechanisms may coexist simultaneously in various disease entities. Figure 137-2 shows the pathological mechanisms of serous subretinal fluid accumulation.

The common and rare conditions that can cause serous detachment of the neural retina are summarized in Box 137-1 .

OCULAR MANIFESTATIONS

Serous, or exudative, retinal detachment typically causes decreased visual function that corresponds to the area of involved retina. Central visual acuity may be intact or may be diminished markedly, and the visual complaints may wax and wane. Patients may complain of metamorphopsia or scotomas accompanied by other complaints such as pain, photophobia, and redness. Photopsias are common and do not necessarily indicate a

 

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Figure 137-1 The normal forces of neural retinal attachment.

retinal break; however, a rhegmatogenous break always must be excluded by careful ophthalmoscopy.

Clinically, serous detachment results in a smooth elevation of the neural retina above the retinal pigment epithelium (RPE). The exudative fluid may be clear or cloudy, shallow or bullous. When bullous, shifting subretinal fluid may occur as the patient’s head position changes, whereas rhegmatogenous retinal detachment does not shift its pattern that readily. This is visualized best with the help of the indirect ophthalmoscope, allowing patients to lie in a dependent position for a few minutes. Sometimes shallow retinal detachments can be observed more easily when a green filter is used on the examining light ( Fig. 137-3 ). In shallow detachments, the fluid may not extend all the way to the ora serrata, although in severe cases, the retina may be so bullous as to contact the posterior lens surface ( Fig. 137-4 ).

Serous detachment of the neural retina caused by local ocular pathology is accompanied by signs of the underlying disease. Vitreous or anterior segment inflammatory cells, external signs of scleritis, exophthalmos, retinal or choroidal vascular abnormalities, congenital disc or retinal abnormalities, choroidal detachments, or intraocular masses may be found along with the exudative fluid.

Below, various disease entities that result in exudative retinal detachment are described. For an in-depth discussion, the reader is referred to the appropriate sections within this book.

Coats’ Disease

Coats’ disease is an idiopathic, presumed congenital disorder of pathological retinal vessel formation that affects predominately boys during the first two decades of life. Abnormal retinal vessels can occur either in the periphery or the central retina and produce extravasation of lipid-rich serum into the surrounding tissues. As increasing leakage occurs, intraretinal and subretinal fluid accumulates. The retina may become bullously detached or, in milder cases, hard exudates accumulate in the macular area. If the retina is detached only shallowly, the characteristic dilated telangiectatic vessels can be confirmed easily with indirect ophthalmoscopy. Fluorescein angiography may be helpful in identifying the “light bulb” appearance of the abnormal vessels and in directing treatment.[4] However, if the retina has elevated bullously with lipid-rich accumulation of subretinal fluid, the diagnosis may be difficult and a differential diagnosis of retinoblastoma should be considered, sometimes necessitating a computed tomography scan if the media are opaque. The features that differentiate Coats’ disease from retinoblastoma are that, in the former disease, the patients are somewhat older, calcium deposition is not seen within the eye, and characteristic retinal vascular abnormalities are present.

In Coats’ disease, destructive therapy directed to the abnormal vessels via trans-scleral cryotherapy or transpupillary laser is effective in inducing gradual resolution of the subretinal fluid.[4] Surgical drainage of the subretinal fluid may be needed simultaneously if the retina is detached bullously. Newer methods of treatment such as radiation therapy, intraocular steroids, and photodynamic therapy are being considered, also, for this disease, although experience is anecdotal. Although the retinal exudates are absorbed completely with time in treated cases, the accompanying amblyopia may limit visual recovery, especially if the condition remains undetected until the child is in school.

 

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Figure 137-2 Pathological processes that result in serous detachment of the neural retina. RPE, Retinal pigment epithelium.

 

 

 

Common and Uncommon Causes of Serous Detachment of the Neural Retina

 

COMMON CONDITIONS

• Coats’ disease

• Central serous chorioretinopathy

• Choroidal tumors

• Postsurgical (associated with choroidal detachments)

• Vogt–Koyanagi–Harada syndrome

• Posterior scleritis

• Exudative age-related macular degeneration

 

UNCOMMON CONDITIONS

• Nanophthalmos

• Uveal effusion syndrome

• Familial exudative vitreoretinopathy

• Orbital inflammation (pseudotumor, cellulitis)

• Infectious retinochoroiditis ((toxoplasmosis, syphilis, cytomegalovirus)

• Sympathetic ophthalmia

• Vasculitis (polyarteritis nodosa, Goodpasture’s syndrome, systemic lupus erythematosus)

• Acute vascular/hemodynamic (hypertensive crisis, toxemia of pregnancy, renal failure)

• Optic nerve pits and colobomas (including morning glory syndrome)

 

 

 

Central Serous Chorioretinopathy (see Chapter 127 )

Central serous chorioretinopathy (CSR) generally affects patients from the third to fourth decades of life. An association has been found with periods of high stress in people with type A, highly anxious personalities. The patients complain of distortion, decreased color sensation, and loss of central vision. The accumulation of subretinal fluid takes place in the macula with secondary pigmentary and RPE changes. Fluorescein angiography often reveals a classic focal point of hyperfluorescence, which may appear like an inverted smoke stack or ink blot. Variations of this classic clinical picture include bullous elevation of the retina with extra macular subretinal fluid and the “hanging teardrop” appearance, in which fluid tracks to the inferior periphery of the eye.

The pathogenesis of CSR has been the subject of debate and conjecture. Fluorescein angiography clearly reveals a focal spot of leakage that originates at the level of the RPE, and fluorescein dye leaks into the subretinal space. However, some reabsorption of fluid must take place from the subretinal space, because the detachment does not enlarge progressively. One theory suggests that the ionic flow is reversed in certain RPE cells and that passive movement of water molecules follows the ions from the choriocapillaris to the subretinal space.[5] Additionally, surrounding RPE cells are not able to absorb all the fluid as rapidly. Focal laser treatment certainly is effective in resolving the detachment associated with CSR, with destruction

 

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Figure 137-3 Serous detachment of the neural retina photographed with green filtered light. A, With the patient in the upright position, fluid is seen along the inferior retinal periphery. B, With the patient in the reclining position, the fluid shifts posteriorly to detach the macula.

 

 

Figure 137-4 Serous detachment of the neural retina secondary to retinoblastoma. A totally detached retina is visible behind the crystalline lens in an eye with an exophytic retinoblastoma. Subretinal tumor foci can be distinguished under the detached retina.

of the source of leakage allowing rapid absorption of the accumulated fluid.

The role of laser in this entity has been debated. Generally, it is accepted that treatment of classic CSR be delayed for a period of 3–4 months to allow for spontaneous resolution, because laser treatment does produce a paracentral scotoma. Additionally, laser treatment does not prevent a recurrence from an adjacent source of leakage. In atypical cases or in recurrences, vision may be impaired markedly, with loss of contrast sensitivity and color discrimination. Earlier focal laser treatment can be contemplated in patients who require rapid rehabilitation, or where the focal area of leakage is located outside the central macula.

Postsurgical Serous Detachment

Fortunately, the incidence of postsurgical serous detachment of the neural retina has decreased substantially due to modern meticulous wound closure. Exudative retinal detachment with associated choroidal detachment currently is seen most frequently in glaucoma procedures that employ a secondary drainage implant, or injection of an antimetabolite, such as mitomycin C, during trabeculectomy.[6] Generally, the retinal detachment subsides with reabsorption of the suprachoroidal fluid; however, detachments associated with a suprachoroidal hemorrhage may take much longer to settle. The pathogenesis of subretinal fluid accumulation is decreased transport of fluid out of the suprachoroidal space. In mild cases, management consists of observation alone, although leaking surgical wounds need to be repaired immediately with drainage of suprachoroidal fluid and restoration of the ocular integrity. Secondary complications, such as corneal endothelial touch, iris prolapse, or choroidal hemorrhage, may have to be corrected with subsequent staged surgery.

Vogt–Koyanagi–Harada Syndrome

The Vogt–Koyanagi–Harada syndrome of ocular inflammation can vary from bilateral iridocyclitis to the full-blown syndrome of choroidal effusion, accumulation of subretinal fluid, optic neuropathy, and meningeal irritation. This entity is seen more commonly in Asians and can prove to be a management dilemma. In one large series, posterior uveitis was present in 75–80% of the eyes that showed evidence of retinal detachment.[7] Systemic corticosteroids are the mainstay of treatment, and early initiation can help to abort the attack. The pathogenesis in this entity, as well as in other types of posterior segment inflammation, is choroidal infiltration with inflammatory cells, destruction of the blood–retina barrier, and vascular leakage into the subretinal space. Immune suppressive agents such as cyclosporin A and methotrexate have been employed successfully in this chronic disease of remissions and flare-ups.

Choroidal Tumors

Solid tumors of the choroid commonly are associated with accumulation of subretinal fluid that produces localized exudative or bullous detachment of the retina. In choroidal melanoma, fluorescein angiography reveals a significant lack of capillary blood supply to the overlying retina along with damage to the RPE cells. Some authors suggest that the metabolic needs of a rapidly growing choroidal tumor outstrip its blood supply, which results in localized ischemia and induced damage in adjacent structures.[8] This explains why subretinal fluid can be associated with a growing choroidal mass and is considered by some to represent a sign of a malignancy in a nevus.

A circumscribed hemangioma of the choroid is a highly vascularized, congenital tumor located close to the disc and macula in most eyes. It manifests during the third to fourth decades of life, with significant leakage associated with its rich vascular supply. Destruction of the overlying RPE impairs the blood–retina barrier, which then allows the large, incompetent choroidal vessels from within the substance of the tumor to leak into the surrounding tissues. Focal grid laser treatment to the surface of a choroidal hemangioma can dry out the associated subretinal fluid by allowing the choriocapillaris to absorb the fluid and by providing a barrier around the margins of the lesion.[9] The benefit of laser therapy is temporary, because the leakage recurs and vision is affected by chronic detachment of the macula. Current means of therapy include low-dose radiation and photodynamic therapy.[9] [10] The diffuse choroidal hemangioma associated with Sturge–Weber’s disease can be extremely difficult to treat, because there is a total exudative detachment of the retina in these eyes and secondary glaucoma is a common complication.

Surface laser treatment of a small choroidal melanoma or nevus to dry out the serous fluid should be contemplated with

 

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Figure 137-5 An intravenous fluorescein angiogram highlights a serous detachment of the neural retina associated with choroidal metastasis. The metastatic tumor to the choroid is visualized along the superotemporal vessels; the fluid extends into the fovea. Note the extensive hyperfluorescence from the surface of the choroidal tumor.

great caution, because rupture of the Bruch’s membrane can lead to a rapid mushroom-shaped growth of the tumor.

Retinoblastomas, especially of the exophytic growth pattern, can produce early, highly bullous detachments of the retina due to the rich vascular supply and rapid increase in size (see Fig. 137-4 ). Systemic chemotherapy with adjuvant local tumor destruction is the treatment of choice and has salvaged many eyes and preserved ambulatory vision. [11] [12] However, if there is vitreous seeding and total retinal detachment, some of these eyes may still need to be enucleated.

The most common primary sites of metastatic carcinoma to the choroid are the breast in female patients and the lung in male patients.[8] Choroidal metastases appear as creamy yellow multi-lobulated lesions and are almost invariably associated with accumulation of subretinal fluid ( Fig. 137-5 ). Physical examination with appropriate ancillary testing spearheaded by an internist is indicated to identify the primary malignancy. If noninvasive testing proves unrewarding in the identification of a primary lesion, then a local choroidal biopsy using a fine-needle aspiration may be employed to determine the cells of origin. Treatment is directed toward the primary tumor with chemotherapy with additional local ocular irradiation. Although radiotherapy may be effective in resolving the subretinal fluid and limiting the growth of the choroidal tumors, the visual prognosis may be limited by the scarring or pigmentary changes in the macula.

Macular Degeneration and Diabetic Retinopathy

Both of these conditions may lead, rarely, to massive exudation from multiple leaking vessels into the subretinal space. The additional presence of elevated serum lipid levels results in a chronic accumulation of fluid with the formation of a macular serous detachment of the neural retina. Treatment is directed toward the choroidal neovascular membrane with thermotherapy or photodynamic laser therapy. In diabetic macular edema, focal laser photocoagulation accompanied by aggressive glycemic and lipid control may help in re-absorption of the exudative fluid.

Rare Conditions That Produce Serous Detachment of the Neural Retina

Nodular or diffuse posterior scleritis consists of painful inflammation of the sclera and associated serous detachment of the choroid and neural retina ( Fig. 137-6 ). This condition can be extremely difficult to treat; fortunately, it is rare. Oral corticosteroids

 

 

 

 

Figure 137-6 Nodular posterior scleritis. A, External appearance. B, The accompanying serous retinal detachment is noted in the inferior retina. (Courtesy of Rand Spencer, MD.)

and anti-metabolites may be indicated to control the inflammation. Other posterior uveitides such as Lyme’s and cat-scratch disease can also produce peri-papillary subretinal fluid accumulation.[13] [14]

Other less common conditions that can result in serous detachment of the retina include orbital cellulitis, orbital arteriovenous malformations, sympathetic ophthalmia, and Wegener’s granulomatosis. In cases of orbital inflammation, the venous outflow from the eye may be compromised by vascular engorgement. This results in exophthalmus, and thereby further vascular compromise. Other systemic circulatory conditions that can produce a rapid breakdown of the blood–retina barrier and exudative retinal detachment include accelerated hypertension, toxemia of pregnancy, and renal failure with acute fluid retention.[15]

Nanophthalmos and idiopathic uveal effusion are rare entities associated with impaired posterior fluid outflow. As a result of thickening of the sclera, the scleral outflow channels become impaired significantly, with a marked decrease in transmission of fluid through the posterior segment. The management of both of these conditions is surgical and consists of making scleral windows to decompress the vortex veins.

Other developmental disorders, such as optic nerve colobomas, morning glory disc, and optic nerve pits, are associated with a combination of retinoschisis and serous detachment of the neural retina.[16] [17] For shallow detachments, demarcating laser treatment can be effective, whereas for larger detachments vitrectomy and gas tamponade may be necessary.

DIAGNOSIS AND ANCILLARY TESTING

Serous separation of the retina can be diagnosed fairly easily with indirect ophthalmoscopy, provided the ocular media is clear. When the media is hazy due to hemorrhage or inflammation,

 

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ancillary testing using ophthalmic ultrasonography or computed tomography scans may provide additional information. Blood tests for a uveitis workup to rule out an infectious cause such as Lyme’s borreliosis, Bartonella infection, and syphilis testing should be considered.

Clinically, the examiner must look carefully for a retinal break to rule out a rhegmatogenous detachment. The vitreous cavity and preretinal surface should be studied for associated traction. A detachment with a rhegmatogenous component has corrugated folds and an opaque appearance of the retina, whereas a serous detachment is smooth and convex in nature. The color of the non-rhegmatogenous detached retina may appear more pink and healthy; however, this feature is difficult to distinguish in longstanding cases. Ocular inflammation, external signs of scleritis, local vascular changes, and lipid-rich subretinal fluid are also helpful in differentiating serous detachment of the neural retina. In longstanding serous detachment of the neural retina, especially when the fluid has waxed and waned, underlying RPE changes—“leopard skin”—are common. Patients who have systemic diseases, such as toxemia of pregnancy and acute renal failure, have the systemic signs associated with these conditions.

Diagnostic Ultrasonography

A diagnostic ultrasonographic evaluation using the “B” scan mode may be extremely helpful for opaque media. Improved tissue resolution with newer ultrasound machines and the ability to image retrobulbar tissues have enhanced diagnostic capabilities. Ultrasonography reveals a convex, dome-shaped collection of subretinal fluid, as well as subretinal fluid that shifts with changes in head position. Local pathology, such as choroidal tumors and scleral inflammation, can be defined fairly easily, and subretinal hemorrhage or other opacities may be better defined, as well.

Computed Tomography and Magnetic Resonance Imaging

These methods of radiological examination of the head and orbits become necessary if retrobulbar orbital pathology is suspected. Radiological investigations may be ordered for an orbital tumor, arteriovenous anastomosis, or exophthalmos. Gadolinium-enhanced magnetic resonance images offer a significant improvement in resolution of the tissue characteristics and may be beneficial in differentiating vascular from infiltrative orbital lesions.

Fluorescein Angiography

Retinal photography and fluorescein angiography can be extremely helpful to establish a source of the subretinal fluid and are necessary if focal laser treatment is contemplated. However, hazy media, vitreous hemorrhage, and bullous retinal detachment may limit the ability of fundus photography to distinguish the cause.

Indocyanine Green Angiography

Digital angiography using indocyanine green dye is a relatively recent innovation. It can be especially helpful to delineate the choroidal vasculature and to detect choroidal pathology in posterior uveitis and central serous chorioretinopathy. [18] In addition, it is possible that the combination of indocyanine green angiography with high-speed video digital imaging may identify abnormal choroidal feeder vessels in vascularized lesions.

Optical Coherence Tomography

Optical coherence tomography (OCT) is an exciting new, noninvasive technique that allows tissue resolution at a cellular level and, thereby, a cell layer–by–cell layer analysis of the ocular

 

 

Figure 137-7 An optic nerve pit with serous detachment of the neural retina involving the central macula. A, A larger area of retinoschisis is present between the arcade vessels. B, Optical coherence tomography of the same eye shows the subretinal fluid under the macula with the larger area of inner retinoschisis.

 

 

 

Differential Diagnosis of Serous Detachment of the Neural Retina

Retinoschisis

 

Traction retinal detachment

 

Rhegmatogenous retinal detachment

 

Choroidal detachment

 

Retinal or subretinal cyst

 

Choroidal or retinal tumor

 

 

 

 

tissues. The ability to resolve the tissue characteristics is helpful in differentiating the hemorrhagic from serous component of age-related macular degeneration. In serous detachment of the neural retina associated with optic nerve pits and colobomas, OCT has shown that no communication exists between the vitreous and the subretinal space. [17] Although the origin of the fluid is yet to be elucidated clearly, tomography findings ( Fig. 137-7 ) do support the hypothesis that the initial elevation of the retina is a schisis-like cavity, followed by a later communication with the subarachnoid fluid. OCT also is helpful in sequential examination of subretinal fluid and to measure the extent of retinal edema.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis is given in Box 137-2 .

TREATMENT

The choice of treatment to resolve the secondary subretinal accumulation of fluid should be directed toward the primary pathology. As discussed above, laser treatment may be effective to treat focal breakdown of the blood–retina barrier, as seen in

 

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central serous chorioretinopathy, exudative diabetic retinopathy, Coats’ disease, or vascular malformations.

Trans-scleral cryotherapy can be considered for peripheral vascular lesions in which the retina is elevated bullously and subretinal fluid does not allow uptake of laser. Diathermy has limitations due to the effects of thinning on the sclera and has mostly fallen out of favor with most retina specialists.

Radiation therapy delivered by means of either an external beam or locally by using an episcleral radioactive plaque can be beneficial in ocular malignancies. Recovery of useful vision in eyes that contain choroidal metastases and even in those with large choroidal hemangiomas (producing a bullous retinal detachment) has been documented. For highly vascularized lesions such as circumscribed choroidal hemangiomas, photodynamic treatment produces a dramatic regression of the tumor and would seem to be the logical choice.[10] However, experience with this modality is limited and long-term outcomes are unknown. Photodynamic therapy is also effective in reducing leakage from occult choroidal neovascularization and capillary hemangiomas, although its visual benefits remain controversial.[19] Trans-pupillary thermotherapy (TTT) is a useful adjunctive therapy for choroidal melanomas after radioactive plaque therapy, as well as for capillary and choroidal hemangiomas, and produces a rapid resolution of accumulated subretinal fluid associated with these tumors. TTT also is being investigated for the treatment of age-related macular degeneration and related occult neovascularization and RPE detachments.

Intra-vitreal steroids delivered by intraocular injection are effective in stabilizing the blood–retina barrier, and various trials have shown their efficacy in macular edema and chronic retinal edema. Similarly, sustained release steroid devices may prove beneficial for chronic conditions such as posterior uveitis and pars planitis.

Systemic treatment with oral or intravenous steroids may be required in cases with bilateral involvement or severe inflammation. Occasionally, systemic anti-metabolite agents may be necessary. Glucocorticoids, anti-inflammatory agents, cyclosporin A, and FK506 (tacrolimus) are powerful drugs with significant systemic toxic effects and, thus, should be used cautiously.

Medical management of a local ocular condition must be carefully coordinated—a physician experienced in the use of oral anti-metabolites and anti-inflammatory agents should be involved in the continued care of the patient.

COURSE AND OUTCOME

The visual outcome and success of therapy for serous detachment of the neural retina is highly dependent on the primary cause. Age of the patient and underlying systemic disease are other important factors. Persistent subretinal fluid does not bode well for long-term visual function. In general, however, the retina seems to tolerate exudative subretinal fluid better than fluid from rhegmatogenous retinal detachment. Therefore, provided the mechanism of fluid accumulation can be altered, good visual outcome can result, even for relatively longstanding macular detachments.

 

 

REFERENCES

 

1. Anand R, Tasman WS. Non-rhegmatogenous retinal detachment. In: Ryan SJ, ed. Retina, vol 3. Surgical retina, ed 3. St Louis: Mosby; 2001.

 

2. Marmor MF, Yao XY. Conditions necessary for the formation of serous detachment. Experimental evidence from the cat. Arch Ophthalmol. 1994;112:830–8.

 

3. Takeuchi A, Kricorian G, Yao XY, et al. The rate and source of albumin entry into saline filled experimental retinal detachments. Invest Ophthalmol Vis Sci. 1994; 35:3792–8.

 

4. Silidor SW, Augsburger JJ, Shields JA, Tasman WS. Natural history and management of advanced Coats’ disease. Ophthalmic Surg. 1988;19:89–93.

 

5. Spitznas M. Pathogenesis of central serous retinopathy: a new working hypothesis. Graefe Arch Klin Exp Ophthalmol. 1986;224:321–4.

 

6. Kokame GT, de Leon MD, Tanji T. Serous retinal detachment and cystoid macular edema in hypotony maculopathy. Am J Ophthalmol. 2001;131:384–6.

 

7. Ohno S, Char DH, Kimura SJ, O’Connor GR. Vogt–Koyanagi–Harada syndrome. Am J Ophthalmol. 1977;83:735–40.

 

8. Shields JA, Shields CL. Intraocular tumors. A text and atlas. Philadelphia: WB Saunders; 1992.

 

9. Shields CL, Honavar SG, Shields JA, et al. Circumscribed choroidal hemangioma: clinical manifestations and factors predictive of visual outcome in 200 consecutive cases. Ophthalmology. 2001;108:2237–48.

 

10. Robertson DM. Photodynamic therapy for choroidal hemangioma associated with serous retinal detachment. Arch Ophthalmol. 2002;120:1155–61.

 

11. Shields CL, Shields JA. Editorial: chemotherapy for retinoblastoma. Med Pediatr Oncol. 2002;38:377–8.

 

12. Shields CL, Shields JA. Recent developments in the management of retinoblastoma. J Pediatr Ophthalmol Strabismus. 1999;36:8–18.

 

13. Krist D, Wenkel H. Posterior scleritis associated with Borrelia burgdorferi (Lyme disease) infection. Ophthalmology. 2002;109:143–5.

 

14. Wade NK, Levi L, Jones MR, et al. Optic disk edema associated with peripapillary serous retinal detachment: an early sign of systemic Bartonella henselae infection. Am J Ophthalmol. 2000;130:327–34.

 

15. Hayreh SS. Systemic arterial blood pressure and the eye. Eye. 1996;10:5–28.

 

16. Lincoff H, Lopez R, Kreissig I. Retinoschisis associated with optic nerve pits. Arch Ophthalmol. 1988;106:61–7.

 

17. Krivoy D, Gentile R, Leibmann JM, et al. Imaging congenital optic disc pits and associated maculopathy using optical coherence tomography. Arch Ophthalmol. 1996;114:165–70.

 

18. Oshima Y, Harino S, Hara Y, Tano Y. Indocyanine green angiographic findings in Vogt–Koyanagi–Harada disease. Am J Ophthalmol. 1996;122:58–66.

 

19. Schmidt-Erfurth UM, Kusserow C, Barbazetto IA, Laqua H. Benefits and complications of photodynamic therapy of papillary capillary hemangiomas. Ophthalmology. 2002;109:1256–66.

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