Exudative Retinal Detachment

Continuing Education Activity

Exudative retinal detachment is multifactorial in origin and can develop in patients of all age groups when there is defective clearance of subretinal fluid or when there is excessive exudation in the subretinal space. Most of the cases may be successfully managed medically. If diagnosed on time and necessary medical and surgical interventions are initiated, reasonably good visual recovery could be achieved. Prompt diagnosis and identification of the cause of exudative retinal detachment can help to avoid high ocular morbidity associated with this condition. This activity reviews the evaluation and management of exudative retinal detachment and highlights the interprofessional team's role in evaluating and treating patients with this condition.

Objectives:

• Identify the etiology and epidemiology of exudative retinal detachment.
• Review the pathophysiology, histopathology, and clinical features of exudative retinal detachment.
• Describe the evaluation, management, and differential diagnoses of exudative retinal detachment.
• Summarize the prognosis, complications, and role of interprofessional collaboration in managing patients with exudative retinal detachment.

Introduction

Accumulating excessive fluid in the subretinal space between the retinal pigment epithelium (RPE) and neurosensory retina leads to retinal detachment (RD).[1] The subretinal space is the remnant of the embryonic optic vesicle.[1] Depending on the etiology which leads to subretinal fluid accumulation, retinal detachment is divided into three categories- rhegmatogenous, tractional, or exudative retinal detachment.[2][3] 

There may be a combination of these categories in some cases. Rhegmatogenous retinal detachment occurs when there are retinal tears or holes leading to fluid seeping into the subretinal space.[4] Tractional retinal detachment occurs when there is traction on the retina due to fibrovascular proliferation over the retina resulting from ischemic or hypoxic stimuli or other causes.[4]

Exudative retinal detachment occurs when excessive subretinal fluid accumulates in the absence of any retinal breaks or tractional forces.[3][4] Exudative retinal detachment occurs due to disruption of the integrity of the blood-retinal barrier.[3]

There is no anatomical adhesion between the retinal pigment epithelium and the neurosensory retina.[1] The apical surface of the retinal pigment epithelial cells expresses neural cell adhesion molecules, which create adhesion between retinal pigment epithelium and photoreceptor cells.[1][5] 

Any etiologic factor, whether inflammatory, idiopathic, infectious, surgical, neoplastic, vascular, or drug-induced, can induce ischemic-hypoxic stimuli, leading to the loss of integrity of the blood-retinal barrier.[6][3]

If diagnosed and treated on time, reasonably good visual acuity can be recovered in patients with exudative retinal detachment.[3] Based on the cause of exudation, exudative retinal detachment is mainly managed on medical lines. Very rarely, if all medical interventions fail, a surgical line of management with scleral buckling or vitrectomy surgery may be considered.[3]

Etiology

Exudative retinal detachment occurs when excess fluid accumulates in the subretinal space either due to hypersecretion of fluid into the subretinal space or defective transport of fluids from the subretinal space. Any inflammatory, idiopathic, infectious, surgical, neoplastic, vascular, or drug-induced etiology can lead to loss of integrity of the blood-retinal barrier, thereby leading to exudative retinal detachment.[6][3] The causes of exudative retinal detachment are as follows-

• Inflammatory[6][7][8]

  • Vogt Koyanagi Harada Syndrome (VKH)[9]
  • Sympathetic Ophthalmia[10][11][12]
  • Orbital Inflammation/ orbital pseudotumor/ idiopathic orbital inflammatory disease[13]
  • Posterior Scleritis[14]
  • Benign reactive lymphoid hyperplasia[15]
  • APMPPE (Acute posterior multifocal placoid pigment epitheliopathy)[16]
  • Serpiginous Choroiditis[17]
  • Behçet disease (BD)[18]
  • Intermediate uveitis[19]
  • Relapsing polychondritis (RPC)[20]
  • Inflammatory bowel disease[21]
  • Sarcoidosis[22]
  • Unilateral acute idiopathic maculopathy[23]
• Idiopathic [24][25]

  • Central serous chorioretinopathy (CSCR)[26]
  • Nanophthamic eyes/ idiopathic uveal effusion[27]
•  Infectious[28][29]

  • Tuberculosis [28]
  • Dengue [30]
  • Syphilis[31]
  • Cat-scratch disease[32]
  • CMV (cytomegalovirus) Retinitis[33]
  • Lyme disease[34]
  • Fungal infection[35]
  • Nematode infection/ Diffuse unilateral subacute neuroretinitis[36] [37]
  • Toxoplasmosis[38]
  • Herpes Zoster[39]
• Surgical or postsurgical[40]

  • Panretinal photocoagulation[40]
  • Scleral buckle[41]
  • Wound leak/hypotony[42]
• Neoplastic or paraneoplastic[43][44]

  • Metastatic disease[45]
  • Choroidal melanoma and nevus[46]
  • Retinoblastoma[47]
  • Choroidal hemangioma[48]
  • Retinal or optic disc capillary hemangioblastoma (Von Hippel-Lindau syndrome)[49]
  • Choroidal osteoma[43]
  • Lymphoma[50]
  • The bilateral diffuse uveal melanocytic proliferation (BDUMP)[51][52]
  • Multiple myeloma[53]
  • Leukemia[54]
  • Lymphomatoid granulomatosis[55]
  • Carcinoma associated retinopathy[56]
• Vascular/Hematologic[57][58][59][60]

  • Toxemia of pregnancy[61]
  • Malignant hypertension[62]
  • Disseminated intravascular coagulation[63]
  • Thrombotic thrombocytopenic purpura[64]
  • Wegener's granulomatosis[65]
  • HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) syndrome[60]
  • Systemic lupus erythematosus [66]
  • Goodpasture syndrome[67]
  • Organ transplantation/hemodialysis[68]
  • Severe diabetic retinopathy, retinal venous occlusion in the systemically unstable patient [69][70]
  • Kidney diseases like IGA nephropathy, chronic renal failure, type II membranoproliferative glomerulonephritis, and crescentic membranous nephropathy.[71]
  • Choroidal neovascularization due to various causes, including age-related macular degeneration (AMD)[72]
  • Idiopathic polypoidal choroidal vasculopathy (IPCV)[73]
  • Coats' disease[74]
  • Retinal vein occlusion[70]
  • Carotid obstruction (venous overload choroidopathy) [75]
  • Familial exudative vitreoretinopathy (FEVR)[76]
  • Retinopathy of prematurity (ROP)[77]
  • Retinal arterial macroaneurysm[78][79]

• Miscellaneous[80][81]

  • Acute exudative polymorphous vitelliform maculopathy[81]
  • Medications like interferon-a, ribavirin, checkpoint inhibitors (atezolizumab, ipilimumab, durvalumab, pembrolizumab, nivolumab, cemiplimab, avelumab), MEK inhibitors, and topiramate.[82][83][84][80]
  • Systemic steroids can cause exudative retinal detachment due to the worsening of CSCR.

Epidemiology

Age predilection in exudative retinal detachment is different for different diseases. Coats disease is commonly seen in the younger age group, exudative retinal detachment secondary to malignancy, exudative age-related macular degeneration is more common in the older age group, exudative retinal detachment secondary to pre-eclampsia, eclampsia, HELLP syndrome, Vogt Koyanagi Harada syndrome, central serous chorioretinopathy is more common in middle age group.[85] 

Choroidal malignancies and exudative age-related macular degeneration are more common in whites.[86][87] The black population has a higher incidence of inflammatory ocular diseases.[88] Vogt Koyanagi Harada syndrome is more common in Asians.[6] Because of the multifactorial origin of exudative retinal detachment, no previous data on the frequency of the disease was available in reviewing the literature. Sex predilection in exudative retinal detachment is also different for different diseases. Central serous chorioretinopathy, Coats disease, and Uveal effusion syndrome are more common in males.[89][27][90] 

Individuals with a stressful lifestyle, type A personality, and pregnancy has a higher incidence of central serous chorioretinopathy.[91]

Pathophysiology

Disruption of the blood-retinal barrier leads to the development of exudative retinal detachment.[92] The key role of the blood-retinal barrier is in managing fluid and molecular transport between retinal vasculature and retinal layers.[93][94] 

The blood-retinal barrier is divided into two categories: the outer blood-retinal barrier and the inner blood-retinal barrier. The outer blood-retinal barrier is formed by the tight junction between the cells of the retinal pigment epithelium.[95] 

No anatomical attachment is present between the retinal pigment epithelium and the neurosensory retina. The apical surface of the retinal pigment epithelial cells has the expression of neural cell adhesion molecules, which help in the attachment between the retinal pigment epithelium and the neurosensory retina.[95] The inner blood-retinal barrier is formed by the tight junction between the endothelial cells of the capillaries.[95] 

Normal functioning of the tight junctions of the cells forming the blood-retinal barrier is responsible for maintaining the integrity of the blood-retinal barrier.[94] If the tight junction is disrupted due to any infective, inflammatory, vascular, infiltrative, neoplastic, or degenerative causes, it leads to failure of the blood-retinal barrier functioning, leading to fluid accumulation in the subretinal space.[92][94] 

Other causes include loss of polarity of retinal pigment epithelium, which causes reversal of pumping and accumulation of fluid in the subretinal space.[91] There is a widening of venous channels and an increase in hydrostatic pressure due to nonperfusion of the choriocapillaris in central serous chorioretinopathy.[96][97]

Histopathology

In the acute stages of exudative retinal detachment, loss of photoreceptor outer segments is seen. In chronic disease, RPE proliferation, cysts, excessive leakage into the subretinal space, and retinoschisis are seen.[3] In the acute stages of Vogt Koyanagi Harada syndrome, eosinophilic exudation is seen in the subretinal space, which disappears in the late stages.[98][99]

Circumscribed choroidal hemangiomas are benign hamartomas that typically present in the second to fourth decade of life. They usually occur sporadically in the absence of systemic disease. Histopathology reveals that the tumor is composed of vascular channels lined with endothelium.[100] 

Choroidal haemangioma shows well-demarcated "pushing" peripheral margins. It is separated from the normal choroid by a layer of choroidal lamellae and compressed melanocytes. While in some cases, the hemangiomas merge with the choroidal vasculature.[101] Diffuse choroidal hemangioma is usually associated with Sturge-Weber syndrome. Orbital pseudotumor presents as an idiopathic inflammation. It consists of pleomorphic inflammatory cellular reactions and a fibrovascular tissue complex. Histopathologic analysis shows a granulomatous inflammation with fibrosis.[102][103] 

Choroidal osteoma shows dense, bony trabeculae with marrow spaces. These spaces are traversed by pathognomonic dilated thin-walled spider or feeder blood vessels. These vessels connect the choriocapillaris to the larger choroidal vessels.[104][105][106] Bilateral Diffuse Uveal Melanocytic Proliferation (BDUMP) shows predominantly spindle-shaped melanocytic cells. These cells are mixed with epithelial cells.[51] These are predominantly spindle-shaped melanocytic cells.[107][108] They are S100 positive.[109] 

On histopathology, multiple myeloma exhibits round plasma cells with an eccentric nucleus and prominent nucleolus. Organized chromatin is present with a clear area next to the nucleus known as Hoffa clear zone. It represents the Golgi apparatus involved in immunoglobulin production.[110] On histopathology, lymphoma shows epidermotropism, which is characteristic of T-cell infiltrates. There is an intraepidermal cluster of lymphocytes known as Pautrier's abscess. It is pathognomic of mycosis fungoides. Angiodestruction and tissue infarction are commonly seen.[111]

History and Physical

Proper assessment of a patient with exudative retinal detachment involves:

• Careful history 
• General physical examination
• Ophthalmic examination

  • Anterior segment examination
  • Posterior segment examination
  • Locating the presence or absence of retinal break or tractional bands.

History

The patient may present with dimness of vision, floaters, pain, visual field defects, redness of the eye, leukocoria, and metamorphopsia. The duration of presenting symptoms should be inquired. Children or rarely ignorant adults may sometimes present with squinting of the eye or leukocoria if unilateral blurring is not noticed early. The history of previous intraocular surgeries and systemic or topical medications (including) should be inquired. History of any associated systemic disease (including hypertension), excessive weight loss, and loss of appetite in suspected cases of malignancy should be thoroughly evaluated. A history of flu-like illness in the prodromal phase is seen preceding the acute uveitic phase of Vogt Koyanagi Harada syndrome.[7] 

General Physical Examination

Exudative retinal detachment is multifactorial in origin. It could occur from local as well as systemic causes. A thorough physical examination is necessary to rule out the systemic causes of exudative retinal detachment like Behçet disease, relapsing polychondritis, Von Hippel-Lindau syndrome, tuberculosis, syphilis, dengue, Lyme disease, cytomegalovirus retinitis, nematode infection, fungal infection, diabetes, hypertension, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome, preeclampsia, eclampsia, hematological malignancies like acute myeloid leukemia, chronic myeloid leukemia, acute lymphoid leukemia, chronic lymphoid leukemia as well as to rule out syndromic associations with exudative retinal detachment.[3]

Ophthalmic Examination

Best-corrected visual acuity should be evaluated. Intraocular pressure should be monitored. The presence of longstanding amblyopia should be ruled out. There may be ptosis, proptosis, and pain in ocular movements in posterior scleritis and orbital inflammation.[112][113]

Anterior Segment Examination

Anterior segment examination may be unremarkable. Inflammatory etiologies are characterized by circumcorneal congestion, aqueous cells, anterior chamber flare, posterior synechiae, complicated cataracts, keratic precipitates, hypopyon, retrolental (anterior vitreous) cells on slit-lamp examination.[114] Raised intraocular pressure may be noted due to secondary angle closure in ciliary congestion and anterior rotation of the ciliary body in scleritis, after pan-retinal photocoagulation, and in VKH syndrome.[16] 

Neovascularization of the iris and angle may be noted in VKH.[115] The pupillary examination should be done to check for RAPD (relative afferent pupillary defect) to assess the severity of the posterior segment involvement.[116] Features of rhegmatogenous retinal detachment, like retrolental pigments (Shafer sign) and hypotony, should be ruled out.[117]

Posterior Segment Examination

Exudative retinal detachment is characterized by the presence of shifting fluid across the retina.[118] As the patient shifts position, the subretinal fluid accumulates in the most dependent area of the retina. Previously shifting fluid was considered to be the hallmark of exudative retinal detachment.[119] However, it is found that shifting fluid is also seen with aphakic and longstanding rhegmatogenous retinal detachment and in patients in whom retinal holes were small.[120] 

Other characteristic features of exudative retinal detachment include the smooth surface of retinal detachment without any retinal folds or corrugations, the convex and bullous contour of retinal detachment, and vitreous cells. Optic disc hyperemia may be seen in inflammatory etiologies causing exudative retinal detachment.[119] Choroidal neovascularization may be seen in chronic non-resolving cases of exudative retinal detachment.[121] 

Choroidal metastases can present with exudative retinal detachment. The choroidal metastases are small in these cases, but the exudative detachment is relatively more.[122][45] There is an absence of associated Shaffer sign, posterior vitreous detachment, and vitreous hemorrhage in exudative retinal detachment contrary to rhegmatogenous retinal detachment.[3] The differences between exudative retinal detachment and rhegmatogenous retinal detachment are discussed in detail in the differential diagnosis section.

Locating the Presence or Absence of Retinal Break or Tractional Bands 

Exudative retinal detachment is a diagnosis of exclusion. So thorough central and peripheral fundus examination is required to rule out the presence of any fibrovascular proliferation causing traction over the retina leading to tractional retinal detachment, or the presence of any retinal tear, hole, or dialysis which may lead to rhegmatogenous retinal detachment.[123][124]

Especially in cases of inferior bullous retinal detachment with shifting fluid, the presence of superior small breaks must be ruled out.[123] If proliferative vitreoretinopathy is present, then it points towards rhegmatogenous retinal detachment. This differentiation is essential as both rhegmatogenous and tractional retinal detachment need a surgical line of management, whereas exudative retinal detachment is primarily managed on medical lines.[125]

Evaluation

Diagnosis of exudative retinal detachment is mainly clinical, but to find out the exact etiology of exudative retinal detachment, further laboratory, radiographic, and other ancillary tests are required.

Laboratory Investigations 

Blood pressure is one of the most important investigations for a patient with papilledema and exudative retinal detachment.

The workup should be individualized and may include a combination of complete blood cell count, differential leukocyte count, erythrocyte sedimentation rate, Mantoux test, chest X-ray, Quantiferon Gold (interferon-gamma release assay), VDRL (venereal disease research laboratory) test, and fluorescein treponema antibody (FTA-ABS) test, serum homocysteine levels, serum cortisol levels, renal function test, liver function test, Toxoplasma, Rubella, Cytomegalovirus, Herpes (TORCH) markers, prothrombin time, bleeding time, clotting time, diabetic profile including fasting blood sugar, postprandial blood sugar, glycosylated hemoglobin.[126] In patients suspected of having BDUMP, evaluation should be done for ovarian cancer, lung carcinoma, and urogenital cancer.[127][128][129] 

Amsler grid is a simple method for the detection of metamorphopsia and scotoma.[130]

 Ocular Imaging

• Optical coherence tomography (OCT) of the macula- OCT scanning shows the macular serous detachment of the macula with or without septae. Enhanced depth imaging OCT shows increased choroidal thickness in VKH syndrome, posterior scleritis, uveal effusion syndrome, and central serous chorioretinopathy.[131] Bacillary layer detachment can be seen in VKH, sympathetic ophthalmia, APMPPE, hematological disorders, posterior scleritis, choroidal metastases, and central serous chorioretinopathy.[132]
• Choroidal thickness decreases as the primary inflammatory insults subside with or without treatment.[133][134] Hence, choroidal thickness is a useful OCT biomarker for disease prognostication.[135] 

In VKH, a thickened choroid is seen on OCT with enhanced depth imaging. There are multiple serous retinal detachments with septa. Choroidal undulation and inward bulging are seen in the acute stage.[136][137]

In CSR on OCT, neurosensory detachment is seen. Hyperreflective dots [in Spectral Domain (SD)-OCT] are seen in the intraretinal and subretinal space.[138][139][140][141] Serous PED is seen in 50% of CSRC-affected eyes.[142][143] Elongation of photoreceptor outer segments is a frequent SD-OCT finding.

In PCV, thumb-like or sharp-peaked pigmentary epithelial detachment (PED) is seen. It signifies the polypoidal lesion at the margin of the PED. Double-layer sign is also present. It is seen as two hyperreflective lines on SD-OCT representing shallow irregular RPE elevation and Bruch's membrane separation due to an abnormal vascular network.[144][145][146]

• Fundus fluorescein angiography (FFA) -It reveals areas of hyperfluorescence and hypofluorescence, multiple window defects, pooling of the dye in the areas of serous retinal detachment, and disc staining.[147] Angiography is also helpful for detecting choroidal neovascularization, neovascularization of the disc, neovascularization elsewhere, retinochoroidal and arteriovenous anastomoses, and for detecting the peripheral ischemic zone to plan for further appropriate lines of management.[148]

In VKH, FFA shows hypofluorescent dots in the early phase, followed by multiple focal areas of leakage and subretinal fluid accumulation in the late phase.[134]

In CSR, an inkblot pattern is seen. There is pinpoint leakage that occurs in the early phase, which then concentrically enlarges in the late phase. In a smokestack pattern, the leakage starts as a pinpoint and gradually expands to form an umbrella-like (or tree-like) appearance.[91]

In Posterior scleritis, FFA shows blocked fluorescence in the initial arteriovenous phase and diffuse hyperfluorescence in the late phase with no leak. Choroidal folds are seen as alternating hyperfluorescent and hypofluorescent bands.[149][150]

In Uveal effusion syndrome, angiography shows hyperfluorescence in a leopard-spot pattern.[151]

In APMPPE, hypofluorescence is seen in the early phase due to the blockage of choroidal fluorescence. Later in the angiogram, there is staining of the lesions. As the process becomes inactive, hyperfluorescence corresponding to window defects in the mottled RPE develops.[152]

In BDUMP FFA early phase shows a reticular pattern of hypofluorescence surrounded by a background of choroidal hyperfluorescence.[153]

• Indocyanine green angiography (ICG) 

In CSR, ICG shows hypocyanescence in the early phase implying choriocapillaris nonperfusion or delayed filling. In the mid-phase, hypercyanescence is seen, indicating choroidal vessel hyperpermeability. This hypercyanescence slowly fades in the late phase.[154][155][156]

In VKH, ICG shows early hyperfluorescence and leakage and hypofluorescent dark dots at the level of the choroid.[157][158]

In IPCV, ICG shows interconnecting channels. An abnormal vascular network appears within 1 min of dye injection. The polyp and feeder vessel are seen.[159][160]

In APMPPE, acute lesions show early hypofluorescence. In the late phases, these lesions become more defined in shape. These areas are more than the placoid lesions seen clinically. As the lesions heal, the hypofluorescence in the late phases becomes small and ill-defined.[161][162][163][164]

• Ultrasonography (B- scan) - Ultrasound is very useful for measuring the dimensions of tumors before and after treatment, measuring choroidal thickness, diagnosis of choroidal detachment, and T sign in posterior scleritis.[112] Ultrasonography is especially useful in patients having hazy media that does not allow posterior segment examination. 

• Autofluorescence (AF) 

Carcinoma Associated Retinopathy (CAR)- On AF, a parafoveal ring of hyper autofluorescence with normal autofluorescence within the ring and hypo autofluorescence outside the ring is seen.[165]

BDUMP- Ultra-widefield color fundus photography shows greater pigmentary changes and lesions in the periphery. Ultra-widefield AF shows the characteristic 'giraffe-pattern' fundus changes.[166]

CSCR- In acute cases, focal areas of hypo-autofluorescence are seen that may correspond to the leak on FFA. In chronic CSCR, hyper-autofluorescent tracks are present due to the accumulation of photoreceptor pigments.[91]

Best disease- AF shows uniform hyper auto fluorescence of vitelliform lesions, while sub-RPE fibrosis or atrophy shows hypofluorescence.[167][168] The increased autofluorescence is due to the lipofuscin content.[169][170][171]

• Electrophysiological tests

Full-field ERG in CAR shows attenuated or absent photopic and scotopic responses. In CAR, where only the cones are affected, full-field ERG could be normal, but multifocal ERG will be abnormal.[172][173]

Treatment / Management

Exudative retinal detachment is multifactorial in origin, so the management approach is individualized depending on the type, severity, and stage of presentation of the disease. Exudative retinal detachment is mainly managed on the medical lines; surgical intervention is rarely indicated if all measures to improve the exudation medically fail.[76]

Inflammatory Diseases like Vogt Koyanagi Harada syndrome and posterior scleritis should be treated with intravenous methylprednisolone pulse therapy at 1 g/day for 3-5 days, followed by a shift to oral steroids according to weight.[7] The role of inflammation and steroid in uveal effusion may be debatable.[27][174]

Along with corticosteroids, immunosuppressive agents such as methotrexate, azathioprine, cyclosporine A, mycophenolate mofetil, and alkylating agents have been used successfully to treat VKH.[175][176][177][178] 

The American Uveitis Society and the International Uveitis Study Group, thus, have recommended immunosuppressive agents as mandatory in treating VKH to prevent recurrences; however, appropriate initial treatment of the disease. While high-dose corticosteroids also affect recurrences, as outlined above, so care must be taken to balance the initial treatment with the need for immunosuppressive agents later on.[7]

Oral nonsteroidal can be effective with various appropriate regimens, such as ibuprofen 600 to 800 mg 4 times daily, piroxicam 20 mg daily, and Naproxen 375 mg twice daily, to name a few. In cases unresponsive to oral NSAIDs (nonsteroidal anti-inflammatory drugs), high-dose systemic corticosteroids are often used, with typical doses of 1 mg/kg/day or approximately 60 mg of prednisone daily.[179][180][181] 

These are tapered slowly over several weeks, carefully considering potential side effects such as weight gain, mood instability, blood-sugar abnormalities, etc. If the patient continues to demonstrate active disease or is unable to tolerate corticosteroids, prompt corticosteroid-sparing immunosuppression is often warranted. Anti-metabolites such as methotrexate and mycophenolate mofetil are employed, often to their maximal doses of 25 mg/week of methotrexate or 1,500 mg twice daily of mycophenolate.[182][180] These medications may take up to six months for full effect, and some patients may require a faster-acting solution. In these cases, biologics such as TNF inhibitors (e.g., adalimumab, infliximab) may be necessary.[183][184]

Malignant hypertensive retinopathy should be managed with the control of blood pressure and the cause of systemic hypertension.

Management options for CSCR include observation, laser, PDT (photodynamic therapy), and anti-VEGF (anti-vascular endothelial growth factor) agents. The RPE leakage sites, as seen on angiography, can be treated with laser photocoagulation. Such therapy seals the leakage point and hastens the resolution of subretinal fluid.[185] 

CSCR with a subfoveal leak, juxtafoveal leak, multiple leaks, and chronic cases with diffuse decompensation of RPE are better managed with PDT.[186][187] Anti-VEGF therapy has been proposed to reduce choroidal hyperpermeability. They upregulate the tight junctions between endothelial cells and the reduction of vascular fenestrations.[188][189][190] Anti

 Surgical intervention is considered the last resort for exudative retinal detachment due to various causes once all efforts to manage the disease medically fail.[2] Options for surgical management include:-[191]

• Scleral buckling with external drainage of the subretinal fluid with the laser of the nonperfused retina
• Pars plana vitrectomy with internal drainage of the subretinal fluid with laser delimitation of the nonperfused retina with or without endotamponade with expansile gases or silicone oil[192][193]

Management of Familial exudative vitreoretinopathy (FEVR) depends on the stage of presentation:[194]

• Stage I FEVR - Observation
• Stage II FEVR - Laser photocoagulation of the areas with abnormal vessels and ischemia (avascular zone)is recommended.[195]
• Advanced stage - In cases of retinal detachment, a surgical approach is required. Scleral buckling and/or vitrectomy, along with lasering of the avascular zone, is recommended. 
• Screening of the family members is advisable.
• A Dexa scan should be done to assess bone mineral density in FEVR patients with LRP5 mutation.[76]
• The use of anti-VEGF is still a matter of debate at present. According to a study by Tagami M. et al., regression of neovascularization was noted after one intravitreal bevacizumab injection.[196]
• A study by Henry CR et al. showed favorable results when intravitreal bevacizumab was used along with laser or surgical treatment.[197]
• There are chances of worsening of tractional forces leading to the tractional retinal detachment on treatment with anti-VEGF injections, so proper guidelines are still awaited for the usage of anti-VEGF as an adjunct to laser or surgical therapy.[197]

Treatment of Coats disease also depends on the stage of the disease.

• Mild cases without exudation can be observed.[20]
• Direct laser photocoagulation of the telangiectatic vessels is useful in mild to moderate cases of exudation.[90]
• Laser therapy will not be effective in cases of massive subretinal exudation and exudative retinal detachment. In such cases, cryotherapy with a double freeze-thaw technique is done over the diseased retina.[198]
• Anti-VEGF medications and intravitreal corticosteroids can be used as adjunctive therapy before laser or surgical management, and they also help to reduce macular edema associated with exudation.[199][200]
• Advanced stages of Coats disease have a very poor visual prognosis. Treatment in advanced stages is aimed at avoiding a painful blind eye and enucleation. Scleral buckling with external drainage or pars plana vitrectomy with or without endotamponade could be attempted to save the eye.[201][191]
• Neovascular glaucoma could be treated with transscleral diode laser photocoagulation.[198]
• Endstage painful blind eye should be enucleated if all measures to save the eye fail.[90]

Exudative retinal detachment due to wound leak or hypotony after ocular surgery responds satisfactorily with timely wound suturing and anti-inflammatory agents coverage.[3] Exudative detachments secondary to pan-retinal photocoagulation or scleral buckling may respond to topical and systemic anti-inflammatory or steroid therapy.[40] If the scleral buckle is too tight, it has to be readjusted to release the pressure on the vascular system.[41]

Radiation therapy is commonly used in the management of malignant uveal melanoma.[46][202] After radiation therapy, especially with proton beam radiation, there are high chances of worsening exudative retinal detachment.[202] Treatment of choroidal tumors with exudative retinal detachment includes proton beam radiation or brachytherapy with plaque, trans retinal tumor biopsy for prognostication of the disease, and surgical intervention as the last measure with pars plana vitrectomy and drainage of subretinal fluid with endotamponade.[46]

Choroidal hemangioma could be treated with various treatment options, including laser photocoagulation, low-dose external beam radiation, proton beam irradiation, gamma knife radiosurgery, radiotherapy, cryotherapy, photodynamic therapy with verteporfin, transpupillary thermotherapy, oral beta-blockers, or intravitreal anti-VEGF.[203] Metastatic tumors should be managed with chemotherapy or focal radiation therapy.[204] 

Infectious causes leading to exudative retinal detachment should be treated with appropriate antibiotics.[205] Tuberculous exudative detachment should be treated with antitubercular drugs along with steroids.[206] Syphilis cause needs to be treated like neurosyphilis with penicillin.[207][208][207] Viral causes warrant urgent treatment with antiviral drugs and corticosteroids.[209] 

Pregnancy-induced hypertension can cause marked loss of visual acuity, but these changes are mostly reversible in the postpartum period.[62] Control of blood pressure is the most important intervention. Visual prognosis is better in pregnancy-induced hypertension as compared to malignant hypertension.[62] 

Secondary exudative retinal detachment in systemic hematologic and vascular etiologies like disseminated intravascular coagulation, malignant hypertension, Goodpasture syndrome, thrombotic thrombocytopenic purpura, post organ transplantation, renal failure, SLE, Wegener's granulomatosis can resolve once the primary disease is controlled and treated.[210] [211][212]

Exudative retinal detachment in hepatitis C patients treated with interferon-a and ribavirin improves with cessation of drugs and initiation of corticosteroid treatment.[80]

Differential Diagnosis

Many conditions can cause exudative retinal detachment. Choroidal pathologies like choroidal melanoma, choroidal lymphoma, choroidal hemangioma, choroidal osteoma, choroidal metastasis, leukemia including ALL (acute lymphoid leukemia), AML (acute myeloid leukemia), CLL (chronic myeloid leukemia), CML (chronic myeloid leukemia).[3] Retinal pathologies like Coats' disease, familial exudative vitreoretinopathy (FEVR), retinal astrocytic hamartoma, vasoproliferative tumor, vitreoretinal lymphoma, retinal vein occlusion, diabetic macular edema. Wet ARMD(age-related macular degeneration), idiopathic macular telangiectasia, thrombotic thrombocytopenic purpura and hemolytic uremic syndrome, pregnancy-induced hypertension including preeclampsia, eclampsia, and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome. 

Miscellaneous causes like central serous chorioretinopathy (CSCR), mitogen-activated protein kinase (MEK) inhibitor-associated retinopathy, uveal effusion syndrome, paraneoplastic retinopathy including acute paraneoplastic polymorphous vitelliform maculopathy (AEPPVM) and bilateral diffuse uveal melanocytic proliferation (BDUMP). 

The causes of exudative retinal detachment, rhegmatogenous retinal detachment (RD), and tractional RD are different. Thus exudative retinal detachment should be differentiated from rhegmatogenous retinal detachment (RD) and tractional RD.

Table

In hemorrhagic retinal detachment, there is subretinal blood compared to an exudative retinal detachment which is serous. Causes of hemorrhagic retinal detachment include peripheral exudative hemorrhagic chorioretinopathy (thought by many authors to be a variant of IPCV), trauma, leukemia, and age-related macular degeneration, specifically in patients on blood thinners.

Prognosis

In exudative retinal detachment secondary to uveitis, the prognosis of the disease depends on the severity of inflammation and its response to treatment.[6] Exudative retinal detachment secondary to uveal effusion and VKH may respond to the high dose of systemic steroids, but the chances of the resurgence of exudation are high.[7][8] Exudative retinal detachment in patients with pre-eclampsia and eclampsia is usually self-limiting and resolves completely with time.[59] 

In patients with Coats disease, the prognosis depends on the severity of macular involvement. Some baseline improvement might occur with treatment but rarely returns to normal visual acuity.[8] Chronic neurosensory detachment and chronic cystoid macular edema may permanently lose cones, leading to limited visual acuity in patients with optic disc pits.[91] 

Patients with acute central serous chorioretinopathy (CSCR) may recover completely, but the chances of recurrences are very high. Once the CSCR becomes chronic, the damage caused to the macula because of recurrent detachments may lead to permanent anatomical alterations in the macular area leading to guarded visual recovery.[24] 

The prognosis of exudative retinal detachment secondary to choroidal tumors depends on the severity and extent of the tumor, presence or absence of macular involvement, response to treatment, chances of recurrence and toxicity, and complications secondary to treatment (radiotherapy, chemotherapy, surgery).[46] 

The exudative retinal detachment secondary to infection such as us tuberculosis, dengue, syphilis, and cat-scratch disease is treated by specific antimicrobial agents with or without steroids. The prognosis is good if the condition is diagnosed and treated early.[213]

Long-standing pathology causes permanent damage to photoreceptors and RPE, and the prognosis is poor even after complete treatment.[214] 

Vascular or haematologic causes such as retinal vein occlusion, carotid obstruction (venous overload choroidopathy), familial exudative vitreoretinopathy, and retinopathy of prematurity can cause exudative retinal detachment. The prognosis is excellent if detected early. Timely laser photocoagulation of the ischaemic retina in familial exudative vitreoretinopathy and retinopathy of prematurity prevent retinal detachment with a good prognosis.[215][195]

Complications

If not treated on time, secondary complications may develop in patients with an exudative retinal detachment.[216] These include:

• Phthisis bulbi[217]
• Neovascular glaucoma,
• Subretinal fibrosis,
• Choroidal neovascularization,
• Pigmentary changes of the fundus,
• Festooned pupil,
• Vitreous hemorrhage, and
• Complicated cataract

Deterrence and Patient Education

The differential diagnosis for exudative retinal detachment is large. Differentiation of exudative, tractional, and rhegmatogenous retinal detachment is of utmost importance and is often achieved through clinical examination alone. In cases of diagnostic query, ultrasonography, fundus fluorescein angiography, indocyanine green angiography, and various laboratory investigations are required for correct diagnosis and treatment. Appropriate and timely intervention by the treating physician may thus help to improve the visual and systemic status of the patient.

Enhancing Healthcare Team Outcomes

Any patient presenting with exudative retinal detachment should not only receive treatment solely by an ophthalmologist in isolation, but it also requires a multispecialty evaluation by a chest physician, radiologist, infectious disease expert, rheumatologist, gastroenterologist, endocrinologist, and the neurologist.[3] Interprofessional communication can lead to better patient management. The patient will most often present to the primary health care provider, including mid-level practitioners, and these professionals should be aware of the condition as it is treatable. A prompt referral to an ophthalmologist is necessary.

These patients can then be followed by their primary clinicians, who should ensure correct dosing on the medication management aspect of the condition. Nursing will be the first department to come in contact with the patients on follow-up and can assess the treatment progress as well as evaluate compliance with both medication and lifestyle measures, and report any issue to the primary care physician. This collaborative, interprofessional team approach to care can ensure optimal patient outcomes.

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Disclosure: Unnati Shukla declares no relevant financial relationships with ineligible companies.

Disclosure: Abhishek Gupta declares no relevant financial relationships with ineligible companies.

Disclosure: Koushik Tripathy declares no relevant financial relationships with ineligible companies.